Innate lymphoid cell

1692: 1073: 1534: 1438: 1330:. ILC2s promote the beiging of adipocytes, and therefore increased energy expenditure. Therefore, decreased responses of ILC2s in the tissue are a characteristic of obesity, as this interrupts their crucial role in energy homeostasis, resulting in reduced energy expenditure and increased adiposity. In addition to ILC2s, ILC1s contribute to the homeostasis of adipose tissue macrophages in both lean and obese conditions, making up 5-10% of the resident lymphocyte population, in human lean adipose depots. A high fat diet increases ILC1 number, and activation of adipose tissue, increasing IFN-γ and TNF-α levels. ILC1s produce the macrophage chemoattractant CCL2, and therefore ILC1- macrophage signalling is a key regulator of adipose tissue. This pathway could be a potential target for treating patients with 1553:. In addition, the number of ILC1s in the intestinal mucosa of patients with Crohn’s disease is increased from approximately 10% to 40% of the total ILCs present. The increase in ILCs present correlates with the severity of the disease. Evidence suggests that the plasticity between ILC3s and ILC1s in the intestine is an important factor of Crohn’s disease, with ILC3s differentiating into ILC1s when exposed to IL-12 produced by dendritic cells. However, IL-23, IL-1B and retinoic acid present in the intestine can drive the differentiation of ILC1s back to ILC3s. Evidence also suggests the ability of ILC2s to acquire the pro-inflammatory phenotype, with ILC2s producing IFN-γ present in the intestine of patients with Crohn’s disease, in response to certain environmental factors such as cytokines. 902:), critical in B and T cell development. Initially it was assumed that ID2 was required in order for CLPs to differentiate into all ILC subsets, however, research showed that knock out of ID2 during CLP development, cripples the development of all ILC subsets other than NK cell progenitors, which are not reliant on the presence of Id2. Due to this realisation, a group of lineage negative cells (requirement of any true precursor cell), that were entirely dependent on the presence of ID2, and expressed other key ILC markers, were identified, with the phenotype: Lin-ID2+IL7Ra+CD25-α4β7+, which are now known as the common helper like innate lymphoid progenitors CHILPs. They are named ‘common helper like’ due to their similarity to the T helper effector cell fates. 1643: 1499: 866: 1635: 1381: 1242: 1021: 743: 1704:(COPD) are a prototypical example of ILC plasticity. Studies in both humans and mice have shown lung resident ILC2s acquire an ILC1 phenotype during COPD, increasing IFN-γ secretion, and therefore inflammation. Various triggers, including cigarette smoke, cause secretion of IL-12 and IL-18, causing the differentiation ILC2s into ILC1s. GATA3 is down-regulated, and T-bet expression is up-regulated. Patients therefore have a higher blood ILC1:ILC2 ratio, with the abundance of ILC1s present correlating with the severity of the disease. 1084:, creating a network between the microbiota, and the host, favouring homeostasis. ILC3s restrict colonization of multiple unbeneficial bacteria in the gut, via secretion of IL-22, stimulating epithelial cells to produce antimicrobial peptides. The IL-22 production is induced due to the production of IL-23 and IL-1β by macrophages and DCs, and it promotes mucosal layer healing. For example, IL-22 can promote repair of intestinal damage after 1666:

Interestingly, it has been suggested that Th17 and Tfh inflammatory responses are generated in the gastrointestinal tract and that microbiota can increase this response. Thus the development of ILCs implicated in regulating the immune response against the microbiota in the intestine has been associated with arthritis. In case of ILC2 has an important role in regulating inflammatory responses by producing IL-4, IL-9, and IL-13.

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common feature in T cells, and it is believed this plasticity is critical to allow our immune system to fine tune responses to so many different pathogens. ILC plasticity requires cytokine receptors, their transcription factors, and access of defined chromatin regions to the transcription factors, however, it still remains unclear where these cytokines are produced and where the differentiation occurs in Vivo.

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inflammatory events. Although the plasticity is reversible, during the differentiation of NKp46+ ILC3s to ILC1, the modulation of the expression of T-bet depends on IL-23, IL-2, and IL-1b and is improved by retinoic acid. Therefore, ILC3 to ILC1 plasticity depends on dendritic cells that produce these cytokines. Although the interconversion of ILC1 and ILC3 is modulated by the differential expression of

191: 767:. They are critical during both the embryonic and adult stages of development of the immune system, and therefore LTi cells are present in organs and tissues early during embryonal development. They have a pivotal role in primary and secondary lymphoid tissue organisation and in adult lymphoid tissue, regulating the adaptive immune response and maintaining secondary lymphoid tissue structures. 1003:. In the intestine, in response to a helminth infection, epithelial cells secrete high levels of IL-25, activating ILC2 cells. ILC2s produce IL-13, which drives the differentiation of additional epithelial cells, via Notch signalling pathways. This instruction allows the tissue to be remodelled to allow for the expulsion of the helminth parasite, and other large pathogens. 1453:, and viruses. These cytokines activate ILC2s, and therefore, an increased number of ILC2s, and type-2 cytokines (IL-4/5/13) are present in patients with allergic asthma. They secrete IL-13, initiating allergic lung inflammation, and additionally promote Th2 differentiation, increasing the production of IL-13, and therefore amplifying the allergic response. 1108:, promoting tolerance to beneficial commensals. The relationship between ILC3s, and T cells in the gut is therefore crucial for maintaining homeostasis, as in the absence of ILC3s, there could be uncontrolled T cell activation. In addition, microbiota play a role in fine tuning IL-22 production by ILC3s, for example, segmented filamentous bacteria in the 1653:, another inflammatory skin disease, causes epidermal thickening, forming plaques which are mainly populated with T cells and dendritic cells. The T cells portray a type 1 immune response; however, the thickening and inflammation of the epidermis is thought to be caused by the production of IL-22, IL-17A, and IL-17F by other T cells such as Th17 or 1457:

ILC2s present correlates with the severity of the disease, and evidence confirms some ‘allergen- experienced’ ILC2s persist after the resolution of the initial inflammation, portraying similarities to memory T cells. The presence of the ‘allergen- experienced’ ILC2s may be the reason asthmatic patients are often sensitised to various allergens.

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vessels and airways. In addition, IL-5-producing ILC2s are found in pulmonary neuroendocrine cells in the airway branch junctions at which particles entering the airways become concentrated. The localization of ILC2 in the airways suggests that the residency of ILC2 is defined by microenvironments in different zones of the tissue.

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expression of gut homing receptors on ILC1s, and ILC3s, and enhances ILC3 function, by upregulating RORγt, and IL-22. There is also crosstalk between macrophages and ILC3s, via RORγt driven GM-CSF production, that is dependent on microbial signalling, and the production of IL-1β by macrophages. A deficiency in dietary

938:. The coordinated expression of these specific transcription factors activate or repress target genes critical in the differentiation of the lymphocyte subsets. In particular, Nfil3, whose expression is regulated by cytokines, controls the differentiation of ILCs via the transcription factors Id2, RORγt, Eomes, and 1406:

of lymphocytes were identified as ILCs, most of them producing IFN-γ ILC1s. ILC3s in the oropharyngeal protect against the infection of Candida albicans producing IL-17A and IL-17F induced by IL-23. Mice lacking ILC3s due to the deletion of RORγt or depletion suffered severe infections by Candida albicans.

734:. NCR- ILC3s mainly produce IL-17A and IL-17F, and under certain circumstances, IL-22. NCR- ILC3s can differentiate into NCR+ upon increased expression levels of T-bet. Despite expressing NK cell markers, ILC3s differ greatly from NK cells, with different developmental pathways and effector functions. 1564:

NK cells secrete IFN-γ, which has anti-tumorigenic effects. Multiple studies show a decreased frequency of NK cells and IFN-γ present in the intestine or peripheral blood of patients with intestinal cancer. Further studies are required to address their exact role in the intestinal cancer environment.

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Evidence suggests that targeting ILCs may be beneficial in the design of therapeutics for autoimmune disorders. As ILCs and T cells have many redundant functions, targeting and neutralizing their effector cytokines might be a better option. Alternatively, targeting their upstream activating mediators

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Although considered homogenous, ILC2s can be classified into subpopulations of natural ILC2s (nILC2s), and inflammatory ILC2s (iILC2s), dependent on their responsiveness to IL-33 and IL-25. nILC2s are those responsive to IL-33 in tissues in a natural immune state, while iILC2s respond to IL-25 or the

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focused on the innate system’s nonspecific nature and lack of memory. As information has emerged about the functions of NK cells and other ILCs as effectors and orchestrators of the adaptive immune response, this distinction has become less clear. Some researchers suggest that the definition should

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In the case of ILC2, Gata3 can be downregulated due to the exposure of infectious agents such as the influenza virus, respiratory syncytial virus, and Staphylococcus aureus, increasing the expression of IL12Rb2, IL-18Ra, and T-bet. The differentiation of ILC2 to ILC1 can also be reversible, although

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The circadian clock and ILC interactions have been demonstrated by studying the regulation of the master gene clock Arntl. Its deletion resulted in the dysregulation of ILC3 caused by epigenetic changes, driving the expression of IL-22 and contributing to the alteration of the microbiome, epithelial

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It has been shown that the ILCs can secrete neurotransmitters and neuropeptides in the lungs. ILC2s interact with neurons in the respiratory tract by the proximity to nerve fibers, and lung resident IL-5-producing ILC2s are found in collagen-rich regions close to the confluence of medium-sized blood

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to induce IL-22 expression, maintaining the number of ILC3s present, and therefore intestinal homeostasis. The vitamin A metabolite, retinoic acid, also upregulates the expression of IL-22, and therefore, the absence of the AhR signalling pathway, and of retinoic acid, results in reduced immunity to

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AHR ligands from diet or microbiota are recognised by immune cells, regulating ILC development and NK cell functions in the intestine. In response to tryptophan metabolites, AhR signalling maintains IL-22 expression and intestinal homeostasis. Retinoic acid, produced by dendritic cells, promotes the

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In addition, ILC1s and ILC3s release oxygen radicals and lethally damaging enzymes in response to pathogenic infection, causing damage to the host tissue. The repair responses for the tissue are coordinated by the type 2 immune response, after the ILC3s and ILC1s have cleansed the tissue of microbes

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In multiple tissue niches, ILCs have a relationship with non- hematopoietic cells such as stromal cells. In the lung, ILC2s have a distinct localization to stromal cells, which release IL-33, and TSLP, promoting ILC2 homeostasis, in both the steady state, and in response to helminth infection, after

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The oral mucosa is colonized with commensals and is exposed to dietary antigens and pathogens. The ILCs in the oral mucosa help maintain the barrier and protect against infections. ILC3s and intraepithelial ILC1s were initially identified in tonsils and found in human gingivae. Approximately 10–15%

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in both mice and humans, via epidermal Notch1 signalling. The ILC3s secrete IL-17F, which plays a role in the immune, and epithelial cellular responses during wound healing, by recruiting macrophages to the site. The expression of TNF also plays a role in wound healing as it directs localization of

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proliferation, and therefore mucus production in the respiratory tract. These functions contribute to the restoration and maintenance of epithelial integrity. ILC2s provide a defence against helminth infections in the lung, via the production of AhR, IL-9, and IL-13. It is believed that these ILC2s

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are the population of ILCs with the most significant anti-tumorigenic potential, with NK cells possessing the ability to recognise missing MHC Class I on the surface of tumor cells. In this way, they act in a complementary manner with the cytotoxic T cells that recognize and kill tumor cells which

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ILCs participate in our immune response to pathogens in all organs, in particular at mucosal surfaces. They are key in the innate immune response due to their ability to rapidly secrete immunoregulatory cytokines, however, they also play a role in the shaping of the adaptive response by interacting

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There are two subsets of ILC3s, NCR- and NCR+ ILC3s, with the displayed NCR on mice ILC3s being NKp46, in comparison to NKp44 displayed on human ILC3s. NKp44+ ILC3s are highly enriched in the tonsils and intestines, as an exclusive source of IL-22. Some ILC3s can also express other NK cell markers,

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The ILCs have been studied in mucosal barriers and their interplay with adaptative immunity, thus implicating them with autoimmune diseases. In arthritis characterized by autoantibodies presence, the dysregulated crosstalk between Tfh and B cells has been implicated in generating those antibodies.

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can also be involved in pro or anti-tumorigenic environments. The production of IL-17 can support the growth of tumors and metastasis since it induces blood vessel permeability, however, the upregulation of MHC Class II on their surface can prime CD4+ T cells, having an anti-tumorigenic effect. In

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between NK cells and ILC1s. Although both cell types use T-bet for development, NK cells have been found to be present in T-bet deficient hosts, but ILC1s are completely dependent on its presence. Development of NK cells is, however, completely dependent on the presence of the transcription factor

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Our understanding of the pathways involved in the development of ILCs has only become clear in the last few years, with our knowledge mainly based on mouse pathways. CLPs have the ability to differentiate into a number of different cell types including T cells, B cells, and ILCs, depending on the

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is frequently observed in response to chronic liver inflammation, and increased proliferation of these ducts is associated with liver cancer. Evidence suggests that the enhanced proliferation is triggered by IL-13, which is produced by IL-33 induced production of ILC2 cells. ILC2s have also been

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The production of IL-5 by ILC2s in the lung leads to eosinophil recruitment, and other cell populations are known to interact and shape the presence of lung ILC2s in airway inflammation in asthmatic patients. In addition, they also promote proliferation of B cells. It is believed the increase in

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ILCs facilitate maintenance of barrier integrity in the intestine, protecting from various bacteria and viral infections. ILC3s are the most abundant subset present in both the adult and foetal intestine. The distribution of ILCs in the intestine changes during development, and they are unevenly

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including T and B cells. CILPs can then differentiate into NK cell precursors (NKP), or the more recently described common helper innate lymphoid progenitors (CHILPs). CHILPs can then differentiate into lymphoid tissue inducer progenitors (LTiPs), and innate lymphoid cell precursors (ILCPs). The

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system, several studies suggest their development and phenotypic maintenance is much more complex, with a high level of plasticity between the subsets. Studies have confirmed the ability of some ILC subsets to convert into a different subset in the presence of specific cytokines. This is also a

1611:, contributing to the development of obesity. Upon dysregulation of homeostasis in the adipose tissue, the decreased responses of ILC2s are a characteristic of obesity, as this interrupts their crucial role in energy homeostasis, resulting in reduced energy expenditure, and increased adiposity. 516:

has been shown to distinguish NK cells from ILC1s. The relationship between the ILC1 and NK cell lineages still remains fuzzy due to a lack of these characteristic markers present on some NK/ILC1 cells in certain tissues, or after certain infection/inflammation events. This supports the tissue

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NK cells express many cell-surface receptors that can be activating, inhibitory, adhesion, cytokine, or chemotactic. The integration of information collected through these numerous inputs allows NK cells to maintain self-tolerance and recognize self-cell stress signals. If the nuanced, dynamic

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How other ILCs impact asthma is less clear, however studies show correlation between the number of IL-17 producing ILC3s, and the severity of the disease. It has been shown in mice that NK cells and ILC1s inhibit ILC2 expansion due to the production of IFN-γ, and therefore may help control the

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triggers inflammation, acting on innate immune cells, including ILC1s, therefore playing an important role in the activation of an inflammatory state in the liver. Therefore, inflammation associated with obesity can influence the progression of liver disease, due to the development of insulin

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due to chronic inflammation, when the ILC3s acquire the ILC1 pro-inflammatory phenotype during chronic inflammation. Since ILCs accumulate in the intestine of IBD patients, it is believed they may have a pro-tumorigenic role. Supporting this, studies show an increase in the amount of effector

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The signaling induced by the cytokines governs the plasticity between ILC3 and ILC1, inducing the expression of T-bet. In patients with Crohn’s disease, the increase of ILC1 at the expense of ILC3 possibly by the production of IL-2 from T regulatory cell, leading to a pathogenic state and

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LTi cells are considered a separate lineage due to their unique developmental pathway, however, they are often considered to be part of the ILC3 group due to their many similar characteristics. Like ILC3s, LTi cells are dependent on RORγt. They are involved in the formation of secondary

142:(inbuilt behavioural changes following a daily cycle). Once matured, the ILCs release cytokines. The classification of ILCs is therefore based on the differences in the transcription factor and cytokine profiles associated with the development and function of the different ILC subtypes. 1424:

cells, and a disrupted uptake of lipids in the intestine. On the other hand, the deletion of Nr1d1, a protein implicated in regulating circadian metabolic responses, resulted in the reduction of NCR+ ILC3 and the increase of IL-17 production, while did not affect the LTi-like ILC3.

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has been shown in vitro, and in vivo. When ILC3s are cultured with IL-2 and IL-15, it causes the up-regulation of T-bet, and the IL-12 receptor (IL-12R) β2, allowing conversion of ILC3s to ILC1s. In addition, studies suggest IL-23 can promote the conversion of ILC1s into ILC3s.

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infection. Retinoic acid also enhances the expression of gut- homing markers on ILC1s, and ILC3s. Dietary nutrient availability therefore modifies the ILC immune response to infection and inflammation, highlighting the importance of a balanced and healthy diet.

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produce cytokines that promote an anti-inflammatory immune response e.g. IL-13, IL-4, Amphiregulin, favouring tumor growth. However, in some settings ILC2s can produce IL-5 promoting a cytotoxic response from eosinophils and therefore an anti-tumor response.

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In the case of ILC3 in multiple sclerosis, these cells have been implicated with tertiary lymphoid aggregates in the brain of patients with progressive disease. In addition, the increase of LTi-like ILC3 correlated with the autoantibodies in the brain fluid.

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distributed throughout the segments of the gastro-intestinal tract. This distribution to different niches within the intestine is mediated through distinct signalling cascades. In humans, approximately 70% of the intestinal ILCs are NCR+, and 15% are NCR-.

1131:, induce IL-22 production by ILC3s. Dendritic cells can also produce IL-23 during pathogen induced stress, also activating ILC3s allowing production of IL-22. One of the mechanisms by which IL-22 regulates microbiota present in the gut is through the 965:

NK cell precursors, and ILC3 precursors have been found in the human tonsil, and foetal ILCPs present in the mouse intestine, accumulating in the Peyer’s Patches. Retinoic acid, produced by many cell types, such as nerve cells, dendritic cells, and

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There is increasing evidence indicating that ILC2s also have a certain degree of plasticity, with studies confirming their ability to convert into ILC1s and ILC3s upon exposure to specific environmental stimuli such as cytokines, or notch ligands.

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to the site, creating an inflammatory environment. If successful, the recruitment of these cells will kill the tumorigenic cells, however in some cases, IFN-γ and TNF-α can play a role in the induction of immunosuppressive immune cells, such as

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ILC2s are tissue resident and involved in the innate response to parasites, such as helminth infection, by helping repair tissue damage. They are abundant in tissues of the skin, lung, liver, and gut. They are characterised by the production of

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Heeren, A. Marijne, et al. "High and interrelated rates of PD-L1+ CD14+ antigen-presenting cells and regulatory T cells mark the microenvironment of metastatic lymph nodes from patients with cervical cancer." Cancer immunology research (2014):

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Since the function of ILCs is linked to their specific tissue localization, determination of the signals involved in their localization and migration patterns will be important in the identification of new avenues for treatment of diseases.

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and IL-23, or pathogenic signals. IL-22 is the principle cytokine produced by ILC3s and plays a fundamental role in maintaining intestinal homeostasis. However, ILC3s produce a variety of other cytokines, including IL-17, IL-22, IFN- γ, and

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All ILC subsets are present in the liver and regulate the immune response to protect the tissue from viral and bacterial infection. ILC1s are the dominant ILC subset present in the liver. Their production of IFN–γ promotes the survival of

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The availability of specific dietary nutrients can affect ILC immune homeostasis by altering the energy stored in the adipose tissue. Adipose tissue maintains metabolism homeostasis and is now considered a fully immunocompetent organ.

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Based on the difference in developmental pathways, phenotype, and signalling molecules produced, in 2013, ILCs were divided into three groups: 1, 2 and 3, however, after further investigation, they are now divided into five groups:

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Lung ILC2s are positioned close to blood vessels, to allow recruitment of eosinophils from the blood. They are also positioned within the airways, where potential pathogens may accumulate. This means they are in close contact with

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The ILCs present in the lungs of patients with COPD, which have the ability to convert into different ILC phenotypes, depending on the microenvironment, which can increase inflammation, contributing to the pathophysiology of the

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Cupedo T, Crellin NK, Papazian N, Rombouts EJ, Weijer K, Grogan JL, et al. (January 2009). "Human fetal lymphoid tissue-inducer cells are interleukin 17-producing precursors to RORC+ CD127+ natural killer-like cells".

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This allergic immune response appears to be independent of T and B cells, with evidence confirming that allergic responses that resembling asthma-like symptoms can be induced in mice that lack T and B cells, using IL-33.

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The strategic positioning and deep rooting of ILCs within tissues allow them to maintain homeostasis, and therefore healthy tissue functioning. However, the ILCs also have detrimental roles in different mucosal sites.

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can dysregulate ILC responses via changes in dietary nutrients, having direct effects on the energy stored in the adipose tissue. Obesity is associated with changes of gastrointestinal flora, increased afflux of free

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Bal SM, Bernink JH, Nagasawa M, Groot J, Shikhagaie MM, Golebski K, et al. (June 2016). "IL-1β, IL-4 and IL-12 control the fate of group 2 innate lymphoid cells in human airway inflammation in the lungs".

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Eomes, whereas ILC1s can develop independent of its presence. This means, Eomes can generally be used as a marker for NK cells, suggesting that mature NK cells are Tbet + Eomes +, and ILC1 are Tbet + Eomes -.

1156:, and deprivation of vitamin A has been shown to enhance ILC2- mediated resistance to helminth infection in mice. ILC3s therefore form a network of interactions to maintain intestinal homeostasis, between the 983:

with other immune cells. The microenvironment of the tissue they reside in determines and fine- tunes the expression of the diverse ILC profiles, facilitating their interaction in multiple effector functions.

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results in abnormally small numbers of ILC3s, and therefore a reduction of IL-22 production, and higher susceptibility to infection. Conversely, retinoic acid suppresses ILC2 proliferation by down regulating

1017:, for epithelial growth factor receptors, which facilitates differentiation of epithelial cells for tissue repair. This can function to enhance the barrier function of the epithelium and slow pathogen entry. 1474:

regulation of NK cell activation becomes unbalanced in favor of attacking self cells, autoimmune disease pathology. NK cell dysregulation has been implicated in a number of autoimmune disorders including

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factors present in the microenvironment determine the progression of CLPs towards specific ILC subtypes, including notch ligands, cytokines, circadian rhythm, and the expression of transcription factors.

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Scordamaglia F, Balsamo M, Scordamaglia A, Moretta A, Mingari MC, Canonica GW, et al. (February 2008). "Perturbations of natural killer cell regulatory functions in respiratory allergic diseases".

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Zhou L, Ivanov II, Spolski R, Min R, Shenderov K, Egawa T, et al. (September 2007). "IL-6 programs T(H)-17 cell differentiation by promoting sequential engagement of the IL-21 and IL-23 pathways".

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from adipose tissue into the liver and increased gut permeability. The close anatomical proximity of the gastrointestinal tract and the liver means transportation of bacterial metabolites through the

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present a foreign antigen on MHC class I. NK cells express a number of cell surface activating NK cell receptors with specificity for stress induced ligands overexpressed on tumor cells. See the

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Gao Y, Souza-Fonseca-Guimaraes F, Bald T, Ng SS, Young A, Ngiow SF, et al. (September 2017). "Tumor immunoevasion by the conversion of effector NK cells into type 1 innate lymphoid cells".

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ILC3s to the damaged skin epidermis. In response to the release of IL-33 by the epidermis, ILC2s secrete high levels amphiregulin, a critical epidermal growth factor, therefore contributing to

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The ILCs present in the nasal polyps of patients with allergic rhinitis, forming a positive feedback loop, promoting inflammation, therefore contributing to the pathophysiology of the disease.

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The ILCs present in the lungs of patients with asthma, and the effector cytokines and cells involved in contributing to the pathophysiology of the disorder, by promoting a Th2 immune response.

1657:. However, more recent data suggests that ILC3s in fact produce a large number of these cytokines, with an increase in the number of ILC3s in the peripheral blood of patients with psoriasis. 1521:

ILC2s are activated due to presence of TSLP and IL-4, produced by epithelial cells and eosinophils respectively. They then produce IL-4, IL-5, and IL-13, further activating eosinophils, in a

1177:, ILC1s and ILC3s cooperate to combat the infection. ILC2s induce goblet cell differentiation, and mucus production in the intestine to protect from tissue damage upon parasitic infection. 821:, the autoimmune regulatory gene, by allowing development of embryonic thymic epithelial cells. They do this via lymphotoxin α4β7 and RANK-L signalling. LTi cells also allow the survival of 1742:

Determining the extent of ILC plasticity during disease could be useful to allow us to prevent or enhance their conversion into other subsets that may be contributing to the pathogenicity.

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loop, promoting inflammation. Disrupting this loop could be a potential therapy for rhinitis. NK cells appear to play a beneficial role, with fewer present in those with allergic rhinitis.

1326:, via the production of IL-5, IL-4 and IL-13. This regulates adiposity, insulin resistance, and caloric expenditure. Dysregulation of this causes persistent type 1 inflammation, leading to 1600:

resistance and metabolic dysregulation. ILC1s as a key regulatory of adipose tissue inflammation, are therefore a potential therapeutic target for treating people with liver disease or

970:, favours the differentiation of ILC3s, rather than ILC2s, and it is required for their complete maturation. In addition, AhR, which can be triggered through ligands produced after the 2003:

Klose CS, Kiss EA, Schwierzeck V, Ebert K, Hoyler T, d'Hargues Y, et al. (February 2013). "A T-bet gradient controls the fate and function of CCR6-RORγt+ innate lymphoid cells".

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The development of ILCs is initiated in response to the presence of transcription factors that are switched on due to the presence of surrounding microenvironmental factors, such as:

668:. iILC2s, express more KLRG1, and reduced Thy1 and ST2. In addition to these subpopulations, another population, named the ILC210 cell, is characterised by its ability to produce 1623:

than in healthy patients. The ILC2s from the skin of the patients had upregulation of the IL-25, IL-33, TSLP and PGD2 receptors, suggesting their role in the activation of ILC2s.

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Zheng Y, Valdez PA, Danilenko DM, Hu Y, Sa SM, Gong Q, et al. (March 2008). "Interleukin-22 mediates early host defense against attaching and effacing bacterial pathogens".

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ILC2s have been confirmed to play a pathogenic role during lung inflammation. Epithelial cells in the lung express the cytokines IL-33 and IL-25, or TSLP, in response to various

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are up-regulated in tissues after infection or injury, and secrete TGFβ1 in tandem with IFN-γ when stimulated. This drives gut epithelial and extra-cellular matrix remodelling.

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ILC1s influence the tumor microenvironment by the production of the cytokines IFN-γ and TNF-α, which at the beginning of immune response polarize other immune cells, such as

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The infection can lead to tissue damage, due to migration of the helminth. ILC2s have a key role in repairing the tissue damage after infection, by producing ligands such as

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Bernink JH, Peters CP, Munneke M, te Velde AA, Meijer SL, Weijer K, et al. (March 2013). "Human type 1 innate lymphoid cells accumulate in inflamed mucosal tissues".

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in adults, as this is where CLPs, NKPs, and CHILPs have been found. The cells then exit and circulate in the blood until they reach their designated tissues, coded for by

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ILC3s and ILC2s are recruited to the wounded dermis in both mice and humans in order to aid in the healing process, by recruiting effector cells to the damaged epidermis.

962:. However, it has also been shown that the maturation of the ILCs can take place outside the primary lymphoid tissues, similar to the maturation of naïve T helper cells. 42:(immune associated), and non- lymphoid tissues, and rarely in the blood. They are particularly abundant at mucosal surfaces, playing a key role in mucosal immunity and 686:

ILC3s are involved in the innate immune response to extracellular bacteria and fungi. They play a key role in homeostasis of the intestinal bacteria and in regulating

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The ILCs present in the epidermis of patients with atopic dermatitis, and the effector cells and cytokines involved in causing the pathophysiology of the disease.

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ILCs and some of their key roles in the intestinal mucosa, allowing maintenance of intestinal homeostasis, via their associated cytokines and effector cells.

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Hepatic ILC1s contribute to pathogenesis of chronic hepatitis B due to the production of IFN-γ, and TNF-α. Disturbance of the epithelium lining the hepatic

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IL-13 also activates T cells, inducing further physiological responses to expel the parasite. T cells stimulate goblet cell mucus secretion, contraction of

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The ILCs present in the epidermis of patients with psoriasis, and the effector cytokines and cells involved in causing inflammation/ epidermal thickening.

1171:, which promotes host commensalism with the local microbiota. ILC1s, and NK cells, produce IFN-γ to combat intracellular pathogens. Upon infection of 445:

Due to ILC1s and NK cells having both shared and unshared features, the classification of human ILC1s has been problematic. Both cell types produce

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cells. ILC1s, are non- cytotoxic or weakly cytotoxic, tissue resident cells, functioning in the defence against infections with viruses and certain

4536:"T helper 2 (Th2) cell differentiation, type 2 innate lymphoid cell (ILC2) development and regulation of interleukin-4 (IL-4) and IL-13 production" 719: 1024:

The different ILC subtypes and how they are implicated in tissue repair and regeneration after infection with oversized organs such as helminths.

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is another good marker for LTi cells in adult mice and humans. They can be either CD4+/-. Like ILC3s, upon activation, LTi cells mostly produce

4838:"Type 1 Innate Lymphoid Cells Protect Mice from Acute Liver Injury via Interferon-γ Secretion for Upregulating Bcl-xL Expression in Hepatocytes" 1537:

The ILCs present in the intestine of patients with IBD, and the effector cytokines and cells contributing to the pathophysiology of the disease.

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A fundamental property of type 2 immunity, and therefore ILC2 cells, is to deal with oversized organisms, that cannot be digested, such as the

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in the bone marrow, so can directly home to the intestine, however, retinoic acid is required to allow CCR9 expression on ILC1s, and ILC3s.

512:

on human ILC1s, which is not present on all NK cells. In addition, NKp80, a marker for human NK cells, is not expressed on ILC1s. In mice,

3078:"Developing lymph nodes collect CD4+CD3- LTbeta+ cells that can differentiate to APC, NK cells, and follicular cells but not T or B cells" 1759:

focus more on the germline-coding of receptors in the innate immune system versus the rearranged receptors of the adaptive immune system.

5418: 5401: 1096:

in the lumen, allowing it to be exposed to lamina propria phagocytes, leading to T cell priming. Although they can present antigens, via

648:. GATA3 is also required for maintenance of ILC2 function, with GATA3 deprivation inhibiting the development and function of the cells. 521:, although expressed by the majority of ILC1s, is absent from the salivary gland resident ILC1s, which also have the ability to express 1233:

addition, ILC3s have been reported to promote the formation of tertiary lymphoid structures in lung cancer, playing a protective role.

838:

cellular signals present. With the exception of NK cells, all ILCs require IL-7 signalling for survival. The transcriptional repressor

1731:

In certain environments, such as inflammation, chronic disease, or tumor microenvironments, activated NK cells can start to express

4109:

Macpherson AJ, Yilmaz B, Limenitakis JP, Ganal-Vonarburg SC (April 2018). "IgA Function in Relation to the Intestinal Microbiota".

1465:

disease. Further research in human patients is required to determine how the balance between the different subsets impacts asthma.

829:, which signal to CD4+ T cells. This role could be used to prevent autoimmunity and to enhance memory responses after vaccination. 355: 6061:"Interleukin-12 and -23 Control Plasticity of CD127(+) Group 1 and Group 3 Innate Lymphoid Cells in the Intestinal Lamina Propria" 5796:"Polarization of ILC2s in peripheral blood might contribute to immunosuppressive microenvironment in patients with gastric cancer" 5637:

Langowski JL, Zhang X, Wu L, Mattson JD, Chen T, Smith K, et al. (July 2006). "IL-23 promotes tumour incidence and growth".

3369:"AHR drives the development of gut ILC22 cells and postnatal lymphoid tissues via pathways dependent on and independent of Notch" 1515: 825:, and therefore memory immune responses, within newly formed lymph nodes. They do this via the TNF superfamily members OX40L and 6405: 5451:"Interleukin-17-producing innate lymphoid cells and the NLRP3 inflammasome facilitate obesity-associated airway hyperreactivity" 5110:"Activation of Type 3 innate lymphoid cells and interleukin 22 secretion in the lungs during Streptococcus pneumoniae infection" 1057:

Intestinal ILCs are exposed to dietary, microbial, and endogenous metabolites. ILC homing to the small intestine is mediated by

5302:"Group 2 innate lymphoid cells are critical for the initiation of adaptive T helper 2 cell-mediated allergic lung inflammation" 931: 4146:"Innate Immune Defenses Mediated by Two ILC Subsets Are Critical for Protection against Acute Clostridium difficile Infection" 1219:

The role of ILC2s and ILC3s in tumor surveillance is dependent on the microenvironment encountered in their resident tissues.

6437: 6295:

Bald T, Wagner M, Gao Y, Koyasu S, Smyth MJ (February 2019). "Hide and seek: Plasticity of innate lymphoid cells in cancer".

1701: 4477:"Characterization of cytokine-induced myeloid-derived suppressor cells from normal human peripheral blood mononuclear cells" 106:, therefore they have been suggested to be the innate counterparts of T cells. The dysregulation of ILCs can lead to immune 2217: 2213:"T-bet and Eomes instruct the development of two distinct natural killer cell lineages in the liver and in the bone marrow" 1792:

Spits H, Cupedo T (2012). "Innate lymphoid cells: emerging insights in development, lineage relationships, and function".

6656: 873:

ILCs are derived from common innate lymphoid progenitors (CILPs), which are derived from CLPs, which have the ability to

405: 4428:"Intraepithelial type 1 innate lymphoid cells are a unique subset of IL-12- and IL-15-responsive IFN-γ-producing cells" 1490:(IL-23, IL-1B, or IL-6), or their survival factors (IL-7) could be used as an approach to treat inflammatory diseases. 1172: 38:, and the regulation of both innate and adaptive immune cells. ILCs are primarily tissue resident cells, found in both 5000:"IL-9-mediated survival of type 2 innate lymphoid cells promotes damage control in helminth-induced lung inflammation" 3821:

Ebbo M, Crinier A, Vély F, Vivier E (November 2017). "Innate lymphoid cells: major players in inflammatory diseases".

1724:

and T-bet, different questions remain that need to be explained to understand the inflammation caused by these cells.

811: 764: 710: 641: 422:

lineages diverge early in their developmental pathways and can be discriminated by their difference in dependence on

90:, and lymphoid tissue inducer (LTi) cells. ILCs are implicated in multiple physiological functions, including tissue 3909:"The orphan nuclear receptor RORgammat directs the differentiation program of proinflammatory IL-17+ T helper cells" 890:, to mediate suppression of the lymphoid cell fates generating T and B cells. It does this via reducing activity of 6692: 5402:"Percutaneous sensitization with allergens through barrier-disrupted skin elicits a Th2-dominant cytokine response" 4585:"Identification of innate IL-5-producing cells and their role in lung eosinophil regulation and antitumor immunity" 846:, yielding an ID2-dependent precursor that can further differentiate with lineage-specific transcription factors. 6339: 1209: 1038: 849:

ILCs are recombination activating gene (RAG)- independent, instead, they rely on cytokine signalling through the

1010:, and they secrete signals recruiting mast cells and eosinophils to the site, stimulating B cell proliferation. 1506:

The frequency of ILC2s has also been found to be elevated in other tissues with allergic symptoms, such as the

430:, and their resident marker expression. NK cells are cytotoxic cells, circulating in the bloodstream, killing 6615: 4378: 783: 731: 602:, which are involved in the distribution of lymphoid cells to specific organ sites. In humans, ILC2s express 59: 5847:"Natural killer cell activity for IFN-gamma production as a supportive diagnostic marker for gastric cancer" 5690:"A human colonic commensal promotes colon tumorigenesis via activation of T helper type 17 T cell responses" 6737: 6707: 6687: 6248:"SMAD4 impedes the conversion of NK cells into ILC1-like cells by curtailing non-canonical TGF-β signaling" 4949:"Adipose Natural Killer Cells Regulate Adipose Tissue Macrophages to Promote Insulin Resistance in Obesity" 2328:"Natural Killer Cells and Type 1 Innate Lymphoid Cells Are New Actors in Non-alcoholic Fatty Liver Disease" 1479: 681: 580: 482: 6246:

Cortez VS, Ulland TK, Cervantes-Barragan L, Bando JK, Robinette ML, Wang Q, et al. (September 2017).

5251:"Immunoregulatory Sensory Circuits in Group 3 Innate Lymphoid Cell (ILC3) Function and Tissue Homeostasis" 3235:"Differentiation of type 1 ILCs from a common progenitor to all helper-like innate lymphoid cell lineages" 481:

produced by both cell types also aid in the eradication of infection. ILC1s and NK cells can also produce

6725: 6720: 6560: 1794: 3274:

Xu W, Domingues RG, Fonseca-Pereira D, Ferreira M, Ribeiro H, Lopez-Lastra S, et al. (March 2015).

1365:

ILC3s are also implicated in lung infections, through the secretion of IL-17, and IL-22, for example in

1300:

ILCs play an important role in maintaining dietary stress, and metabolic homeostasis. The production of

1153: 942:. This provides evidence for the tissue signals playing a key role in fate decisions into ILC lineages. 910:

Each stage of differentiation is dependent on expression of different transcription factors, including:

791: 518: 509: 4583:

Ikutani M, Yanagibashi T, Ogasawara M, Tsuneyama K, Yamamoto S, Hattori Y, et al. (January 2012).

1578:

shown to enhance the progression of liver fibrosis, in turn promoting the development of liver cancer.

1546: 603: 508:

in both humans and mice. They also have differences in phenotypic markers, including the expression of

31: 6410: 5999:"Expansion of human NK-22 cells with IL-7, IL-2, and IL-1beta reveals intrinsic functional plasticity" 6430: 6395: 1305: 935: 895: 6059:

Bernink JH, Krabbendam L, Germar K, de Jong E, Gronke K, Kofoed-Nielsen M, et al. (July 2015).

3907:

Ivanov II, McKenzie BS, Zhou L, Tadokoro CE, Lepelley A, Lafaille JJ, et al. (September 2006).

3580:

Dahlgren MW, Jones SW, Cautivo KM, Dubinin A, Ortiz-Carpena JF, Farhat S, et al. (March 2019).

2684:"The transcription factor GATA3 is essential for the function of human type 2 innate lymphoid cells" 1683:

Our classification of ILCs into subsets provides a simplified framework, however, despite the above

4204:

Wagner M, Moro K, Koyasu S (May 2017). "Plastic Heterogeneity of Innate Lymphoid Cells in Cancer".

1957:

Walker JA, Barlow JL, McKenzie AN (February 2013). "Innate lymphoid cells--how did we miss them?".

1483: 1366: 1185:

Different groups of innate lymphoid cells have ability to influence tumorigenesis in several ways.

3320:"Identification and distribution of developing innate lymphoid cells in the fetal mouse intestine" 34:(CLPs). In response to pathogenic tissue damage, ILCs contribute to immunity via the secretion of 6764: 5501:

Vivier E, Raulet DH, Moretta A, Caligiuri MA, Zitvogel L, Lanier LL, et al. (January 2011).

5300:

Halim TY, Steer CA, Mathä L, Gold MJ, Martinez-Gonzalez I, McNagny KM, et al. (March 2014).

4998:

Turner JE, Morrison PJ, Wilhelm C, Wilson M, Ahlfors H, Renauld JC, et al. (December 2013).

4890:

Brestoff JR, Kim BS, Saenz SA, Stine RR, Monticelli LA, Sonnenberg GF, et al. (March 2015).

4728:"NCR(+)ILC3 concentrate in human lung cancer and associate with intratumoral lymphoid structures" 4726:

Carrega P, Loiacono F, Di Carlo E, Scaramuccia A, Mora M, Conte R, et al. (September 2015).

4000:

Ibiza S, García-Cassani B, Ribeiro H, Carvalho T, Almeida L, Marques R, et al. (July 2016).

2527:

Kim BS, Siracusa MC, Saenz SA, Noti M, Monticelli LA, Sonnenberg GF, et al. (January 2013).

2144:

Jowett GM, Norman MD, Yu TT, Rosell Arévalo P, Hoogland D, Lust ST, et al. (February 2021).

1907: 1200: 611: 135: 5739:"Adenoma-linked barrier defects and microbial products drive IL-23/IL-17-mediated tumour growth" 2723:

Juelke K, Romagnani C (February 2016). "Differentiation of human innate lymphoid cells (ILCs)".

1212:, and therefore anti-inflammatory cytokines, allowing an immune environment the tumor cells can 1135:

patterns of epithelial cells. IL-22, and lymphotoxin expression by ILC3s controls expression of

6800: 6607: 5737:

Grivennikov SI, Wang K, Mucida D, Stewart CA, Schnabl B, Jauch D, et al. (November 2012).

1755: 1359: 1310: 1259: 1116: 955: 4782:"Type 2 Innate Lymphoid Cells in Liver and Gut: From Current Knowledge to Future Perspectives" 2682:

Mjösberg J, Bernink J, Golebski K, Karrich JJ, Peters CP, Blom B, et al. (October 2012).

2578:"Cutaneous immunosurveillance and regulation of inflammation by group 2 innate lymphoid cells" 2377:

Weizman OE, Adams NM, Schuster IS, Krishna C, Pritykin Y, Lau C, et al. (November 2017).

1829:

Spits H, Artis D, Colonna M, Diefenbach A, Di Santo JP, Eberl G, et al. (February 2013).

6646: 6623: 6599: 5200:

Vivier E, Artis D, Colonna M, Diefenbach A, Di Santo JP, Eberl G, et al. (August 2018).

5051:"S1P-dependent interorgan trafficking of group 2 innate lymphoid cells supports host defense" 3367:

Lee JS, Cella M, McDonald KG, Garlanda C, Kennedy GD, Nukaya M, et al. (November 2011).

2101:

Vivier E, Artis D, Colonna M, Diefenbach A, Di Santo JP, Eberl G, et al. (August 2018).

1592: 1372:. Further studies are required to decipher the role of ILCs in human respiratory infections. 1314: 869:

Schematic diagram of the development of ILCs, mainly based on mouse differentiation pathways.

485:, further contributing to the inflammatory response, depending on their molecule expression. 218: 46:. Characteristics allowing their differentiation from other immune cells include the regular 5449:

Kim HY, Lee HJ, Chang YJ, Pichavant M, Shore SA, Fitzgerald KA, et al. (January 2014).

4287:"Cancer Immunosurveillance by Tissue-Resident Innate Lymphoid Cells and Innate-like T Cells" 4285:

Dadi S, Chhangawala S, Whitlock BM, Franklin RA, Luo CT, Oh SA, et al. (January 2016).

4060:

Goto Y, Obata T, Kunisawa J, Sato S, Ivanov II, Lamichhane A, et al. (September 2014).

2529:"TSLP elicits IL-33-independent innate lymphoid cell responses to promote skin inflammation" 6795: 6487: 6423: 6010: 5750: 5646: 5514: 5062: 4903: 4739: 4013: 3536: 2771: 2638: 2159: 2014: 1768: 1751: 1608: 1213: 1124: 818: 638: 423: 286: 27: 4122: 2971:

Takatori H, Kanno Y, Watford WT, Tato CM, Weiss G, Ivanov II, et al. (January 2009).

1807: 1254:. The production of IFN-γ by ILC1s is dependent on the expression of the NK cell receptor 465:

co-stimulation also significantly increases IFN-γ levels. The release of IFN-γ stimulates

8: 6679: 6518: 4892:"Group 2 innate lymphoid cells promote beiging of white adipose tissue and limit obesity" 4426:

Fuchs A, Vermi W, Lee JS, Lonardi S, Gilfillan S, Newberry RD, et al. (April 2013).

4002:"Glial-cell-derived neuroregulators control type 3 innate lymphoid cells and gut defence" 2758:

Buonocore S, Ahern PP, Uhlig HH, Ivanov II, Littman DR, Maloy KJ, Powrie F (April 2010).

1550: 1193: 1072: 1058: 1034: 1029:

the helminth has developed in the intestine, and migrated to the lung through the blood.

478: 419: 75: 6400: 6102:"Cutting Edge: Notch Signaling Promotes the Plasticity of Group-2 Innate Lymphoid Cells" 6014: 5754: 5650: 5518: 5066: 4907: 4743: 4017: 3540: 2775: 2642: 2163: 2018: 1642: 1354:

ILC1s and NK cells secrete IFN-γ in response to viral infection in the lungs, including

746:

The different phenotypic markers present on LTi cells present in an embryo and an adult.

6651: 6638: 6370: 6320: 6272: 6247: 6228: 6185: 6128: 6101: 6033: 5998: 5979: 5925: 5900: 5873: 5846: 5822: 5795: 5771: 5738: 5714: 5689: 5670: 5583: 5535: 5502: 5475: 5450: 5431: 5377: 5352: 5328: 5301: 5277: 5250: 5231: 5177: 5150: 5108:

Van Maele L, Carnoy C, Cayet D, Ivanov S, Porte R, Deruy E, et al. (August 2014).

5085: 5050: 5026: 4999: 4975: 4948: 4924: 4891: 4864: 4837: 4808: 4781: 4703: 4676: 4560: 4535: 4501: 4476: 4452: 4427: 4408: 4359: 4311: 4286: 4267: 4172: 4145: 4086: 4061: 4034: 4001: 3982: 3938: 3889: 3846: 3753: 3726: 3707: 3659: 3632: 3608: 3581: 3557: 3524: 3495: 3468: 3444: 3417: 3393: 3368: 3344: 3319: 3207: 3180: 3143: 3118: 2999: 2972: 2950: 2901: 2874: 2841: 2816: 2792: 2759: 2659: 2626: 2625:

Neill DR, Wong SH, Bellosi A, Flynn RJ, Daly M, Langford TK, et al. (April 2010).

2602: 2577: 2553: 2528: 2504: 2477: 2405: 2378: 2354: 2327: 2292: 2265: 2241: 2212: 2211:

Daussy C, Faure F, Mayol K, Viel S, Gasteiger G, Charrier E, et al. (March 2014).

2193: 2180: 2145: 2038: 1982: 1931: 1902: 1860: 1654: 1601: 1561:

cytokines IL-23, IL-17, and IL-22, in the tumor microenvironment of intestinal cancer.

1475: 1136: 1128: 950:

Studies suggest primary site of ILC development is in the liver in the foetus, and the

850: 714: 599: 119: 3094: 3077: 2430:"Cutting edge: Salivary gland NK cells develop independently of Nfil3 in steady-state" 1351:

originate in the intestine and migrate into the lung to fight the helminth infection.

974:

food, is required for the maintenance of function and expression of intestinal ILC3s.

6702: 6583: 6502: 6482: 6362: 6324: 6312: 6277: 6220: 6189: 6177: 6133: 6082: 6038: 5971: 5930: 5878: 5827: 5776: 5719: 5688:

Wu S, Rhee KJ, Albesiano E, Rabizadeh S, Wu X, Yen HR, et al. (September 2009).

5662: 5619: 5575: 5540: 5480: 5423: 5382: 5333: 5282: 5223: 5182: 5131: 5090: 5031: 4980: 4929: 4869: 4813: 4757: 4708: 4657: 4624:

Wagner M, Ealey KN, Tetsu H, Kiniwa T, Motomura Y, Moro K, Koyasu S (February 2020).

4606: 4565: 4506: 4457: 4400: 4383: 4363: 4351: 4316: 4271: 4259: 4221: 4177: 4144:

Abt MC, Lewis BB, Caballero S, Xiong H, Carter RA, Sušac B, et al. (July 2015).

4126: 4091: 4039: 3974: 3930: 3881: 3838: 3758: 3699: 3664: 3613: 3562: 3500: 3449: 3398: 3349: 3297: 3256: 3212: 3148: 3099: 3058: 3004: 2942: 2906: 2846: 2797: 2740: 2705: 2664: 2607: 2558: 2509: 2451: 2410: 2359: 2297: 2246: 2197: 2185: 2126: 2030: 1974: 1936: 1852: 1811: 1620: 1557: 1522: 1204: 6374: 6100:

Zhang K, Xu X, Pasha MA, Siebel CW, Costello A, Haczku A, et al. (March 2017).

5587: 5435: 5235: 4412: 3986: 3893: 2954: 1986: 6575: 6551: 6354: 6304: 6267: 6259: 6212: 6167: 6123: 6113: 6072: 6028: 6018: 5963: 5920: 5912: 5868: 5858: 5817: 5807: 5766: 5758: 5709: 5701: 5674: 5654: 5611: 5567: 5558:

Baxter AG, Smyth MJ (February 2002). "The role of NK cells in autoimmune disease".

5530: 5522: 5470: 5462: 5413: 5372: 5364: 5323: 5313: 5272: 5262: 5213: 5172: 5162: 5121: 5080: 5070: 5021: 5011: 4970: 4960: 4919: 4911: 4859: 4849: 4803: 4793: 4747: 4698: 4688: 4647: 4637: 4596: 4555: 4547: 4496: 4488: 4447: 4439: 4392: 4343: 4306: 4298: 4251: 4213: 4167: 4157: 4118: 4081: 4073: 4029: 4021: 3966: 3942: 3920: 3873: 3850: 3830: 3748: 3738: 3711: 3691: 3654: 3644: 3603: 3593: 3552: 3544: 3490: 3480: 3439: 3429: 3388: 3380: 3339: 3331: 3287: 3276:"NFIL3 orchestrates the emergence of common helper innate lymphoid cell precursors" 3246: 3233:

Klose CS, Flach M, Möhle L, Rogell L, Hoyler T, Ebert K, et al. (April 2014).

3202: 3192: 3138: 3130: 3089: 3048: 2994: 2984: 2934: 2896: 2886: 2836: 2828: 2787: 2779: 2732: 2695: 2654: 2646: 2597: 2589: 2548: 2540: 2499: 2489: 2441: 2400: 2390: 2349: 2339: 2287: 2277: 2236: 2226: 2175: 2167: 2150: 2116: 2042: 2022: 2005: 1966: 1926: 1916: 1864: 1842: 1803: 1732: 1628: 1168: 756: 687: 537: 446: 139: 39: 5983: 4947:

Lee BC, Kim MS, Pae M, Yamamoto Y, Eberlé D, Shimada T, et al. (April 2016).

4334:

Cerwenka A, Lanier LL (October 2001). "Natural killer cells, viruses and cancer".

2760:"Innate lymphoid cells drive interleukin-23-dependent innate intestinal pathology" 2627:"Nuocytes represent a new innate effector leukocyte that mediates type-2 immunity" 1518:. The concentration of ILC2s positively correlates with severity of the diseases. 1498: 886:

The development of CLPs to CILPs and on to ILCs requires the transcription factor

587:. Due to their cytokine signature, they are considered the innate counterparts of 6567: 6232: 6077: 6060: 5318: 4854: 4642: 4625: 4443: 4217: 3598: 3434: 3292: 3275: 3134: 2700: 2683: 2544: 2494: 1542: 1343: 214: 55: 51: 6154:

Meininger I, Carrasco A, Rao A, Soini T, Kokkinou E, Mjösberg J (October 2020).

4242:

Wagner M, Koyasu S (May 2019). "Cancer Immunoediting by Innate Lymphoid Cells".

2576:

Roediger B, Kyle R, Yip KH, Sumaria N, Guy TV, Kim BS, et al. (June 2013).

2478:"Innate Lymphoid Cells: Diversity, Plasticity, and Unique Functions in Immunity" 6308: 6003:

Proceedings of the National Academy of Sciences of the United States of America

5615: 5218: 5201: 4965: 4551: 4302: 4162: 3925: 3908: 3631:

Sui P, Wiesner DL, Xu J, Zhang Y, Lee J, Van Dyken S, et al. (June 2018).

3251: 3234: 2395: 2121: 2107: 2102: 1437: 1323: 1101: 1042: 1000: 807: 691: 669: 576: 572: 462: 458: 454: 399: 395: 365: 324: 320: 305: 267: 237: 226: 180: 176: 67: 5916: 5863: 5571: 3053: 3036: 2736: 2171: 1020: 759:

by promoting lymphoid tissue development, which they do through the action of

16:

Group of innate immune cells that are derived from common lymphoid progenitors

6789: 6774: 6756: 6594: 6556: 6477: 6172: 6155: 6118: 5901:"Functional interactions between innate lymphoid cells and adaptive immunity" 5845:

Lee J, Park KH, Ryu JH, Bae HJ, Choi A, Lee H, et al. (September 2017).

5368: 5267: 5167: 4693: 4601: 4584: 4492: 4255: 3743: 3582:"Adventitial Stromal Cells Define Group 2 Innate Lymphoid Cell Tissue Niches" 3485: 2891: 2446: 2429: 2344: 2282: 1921: 1331: 1132: 1105: 1007: 874: 843: 822: 771: 634: 588: 568: 564: 541: 474: 368: 347: 271: 263: 259: 95: 6023: 5526: 5419:

10.1002/(SICI)1521-4141(199803)28:03<769::AID-IMMU769>3.0.CO;2-H

5126: 5109: 5075: 5049:

Huang Y, Mao K, Chen X, Sun MA, Kawabe T, Li W, et al. (January 2018).

4836:

Nabekura T, Riggan L, Hildreth AD, O'Sullivan TE, Shibuya A (January 2020).

4677:"The Interplay Between Innate Lymphoid Cells and the Tumor Microenvironment" 4626:"Tumor-Derived Lactic Acid Contributes to the Paucity of Intratumoral ILC2s" 4381:(April 2001). "A fresh look at tumor immunosurveillance and immunotherapy". 4077: 3649: 3197: 3181:"Innate lymphoid cells. Innate lymphoid cells: a new paradigm in immunology" 2973:"Lymphoid tissue inducer-like cells are an innate source of IL-17 and IL-22" 2875:"Group 3 ILCs: Peacekeepers or Troublemakers? What's Your Gut Telling You?!" 1708: 1691: 1380: 1241: 6589: 6497: 6492: 6366: 6316: 6281: 6224: 6181: 6137: 6086: 6042: 5975: 5934: 5882: 5831: 5780: 5723: 5666: 5623: 5579: 5544: 5484: 5386: 5337: 5286: 5227: 5186: 5135: 5094: 5035: 4984: 4933: 4873: 4817: 4761: 4712: 4661: 4610: 4569: 4510: 4461: 4404: 4355: 4320: 4263: 4225: 4181: 4130: 4095: 4043: 3978: 3934: 3885: 3842: 3762: 3703: 3668: 3617: 3566: 3504: 3453: 3402: 3353: 3301: 3260: 3216: 3152: 3062: 3008: 2946: 2910: 2850: 2801: 2744: 2709: 2668: 2611: 2562: 2513: 2455: 2414: 2363: 2301: 2250: 2189: 2130: 2034: 1978: 1940: 1856: 1815: 1634: 1627:

and mast cells are also present in these skin lesions, producing IL-4, and

1583: 1286: 1143:

of epithelial cells, providing a nutrient source for the luminal bacteria.

1140: 1097: 1093: 1089: 1085: 1014: 967: 854: 560: 522: 427: 338: 290: 222: 5812: 5427: 4108: 3103: 1528: 6769: 6472: 6467: 5016: 4798: 4652: 4062:"Innate lymphoid cells regulate intestinal epithelial cell glycosylation" 2989: 2266:"T-bet and Eomesodermin in NK Cell Development, Maturation, and Function" 2231: 1596: 1507: 1347: 1278: 1274: 1258:. IL-12-driven IFN-γ production by ILC1s is accelerated by extracellular 951: 799: 760: 699: 584: 391: 331: 91: 43: 5762: 5658: 4915: 4025: 3834: 3548: 2783: 2650: 2026: 865: 6446: 4752: 4727: 3469:"Innate Lymphoid Cells in Helminth Infections-Obligatory or Accessory?" 2379:"ILC1 Confer Early Host Protection at Initial Sites of Viral Infection" 1619:

The frequency of ILC2s is higher in the inflamed skin of patients with

1355: 1301: 1251: 1164: 1157: 1120: 971: 779: 752: 694:

of the intestine, and the tonsils, however, they are also found in the

466: 99: 47: 5600: 713:

for their development and function. They express RORγt in response to

496:

ILC1s and NK cells have some phenotypic markers in common, including:

6742: 6697: 6545: 4347: 2817:"The IL-23-IL-17 immune axis: from mechanisms to therapeutic testing" 1650: 1574: 1511: 1245:

The different ILC subtypes and how they are implicated in metabolism.

1148: 959: 595: 470: 205: 198: 63: 6358: 6263: 6216: 5967: 5705: 5466: 4835: 4582: 3695: 3384: 3335: 2938: 2832: 2593: 1970: 1847: 1830: 1533: 1160:, intestinal epithelium, neuro-glial cells, and other immune cells. 6511: 6462: 6340:"Shades of grey--the blurring view of innate and adaptive immunity" 6245: 3970: 3877: 1624: 1587: 1549:

due to their increased abundance in the intestine of patients with

1446: 1282: 1112:

regulate IL-22 production and allow differentiation of Th17 cells.

881: 533: 529: 439: 208: 131: 35: 5503:"Innate or adaptive immunity? The example of natural killer cells" 4725: 4396: 3999: 3633:"Pulmonary neuroendocrine cells amplify allergic asthma responses" 3273: 544:, due to the sole production of IFN-γ without cytotoxic activity. 6730: 5794:

Bie Q, Zhang P, Su Z, Zheng D, Ying X, Wu Y, et al. (2014).

1773: 1327: 703: 513: 449:

as their principle cytokine and require the transcription factor

111: 6202: 2428:

Cortez VS, Fuchs A, Cella M, Gilfillan S, Colonna M (May 2014).

1196:

page for further information on NK cells in tumor surveillance.

1119:

to maintain intestinal homeostasis, as in response to bacteria,

1041:. Other studies also confirm the regulation of ILC function via 742: 6533: 6454: 4284: 1739:, common ILC1 markers, strengthening their plastic properties. 1541:

Research suggests IL-17 producing NCR- ILC3s contribute to the

1450: 1389: 1267: 927: 695: 661: 453:

to do so. Both cells can also produce IFN-γ when the cytokines

351: 328: 168: 115: 103: 102:, repair, and regeneration. Many of their roles are similar to 6415: 6196: 6058: 2681: 6396:

Innate lymphoid cells: major players in inflammatory diseases

2923: 1736: 1294: 1290: 1263: 1255: 1109: 1081: 923: 915: 911: 899: 891: 826: 803: 787: 665: 645: 627: 619: 615: 607: 497: 450: 435: 431: 375: 361: 312: 301: 282: 251: 241: 183: 5736: 5500: 5199: 3681: 3178: 2143: 2100: 1831:"Innate lymphoid cells--a proposal for uniform nomenclature" 1388:

Evidence shows ILC3s and ILC2s are recruited to the wounded

875:

differentiate into a number of different lymphoid cell types

4997: 3579: 2376: 1828: 1394: 1062: 919: 795: 775: 727: 657: 623: 553: 505: 501: 383: 275: 244: 87: 83: 5107: 3906: 1273:

NK cells play a role in the immune response against viral

6153: 3179:

Eberl G, Colonna M, Di Santo JP, McKenzie AN (May 2015).

2757: 2427: 2146:"ILC1 drive intestinal epithelial and matrix remodelling" 2002: 939: 887: 839: 778:, and the cytokines IL-1B, IL-23, and IL-6. They express 540:, whereas ILC1s are considered the innate counterpart of 387: 190: 6054: 6052: 5687: 5350: 4674: 3366: 2970: 234:

Large extracellular molecules (parasites and allergens)

5952: 5636: 5594: 3993: 3522: 2263: 1529:

Inflammatory bowel disease (IBD), and intestinal cancer

994: 4668: 4623: 4474: 4143: 3863: 2575: 737: 6049: 5894: 5892: 5351:

Oboki K, Nakae S, Matsumoto K, Saito H (April 2011).

4889: 4831: 4829: 4827: 4059: 3820: 3727:"Metabolic Control of Innate Lymphoid Cell Migration" 3232: 3075: 2815:

Gaffen SL, Jain R, Garg AV, Cua DJ (September 2014).

2624: 2326:

Luci C, Vieira E, Perchet T, Gual P, Golub R (2019).

2325: 1289:. They eliminate hepatic cells in fibrotic liver via 536:, NK cells are considered the innate counterparts of 6149: 6147: 5448: 5399: 4425: 4102: 3955: 2966: 2964: 2868: 2866: 2864: 2862: 2860: 2526: 2210: 1956: 1556:

Patients with IBD have an increased risk of getting

489: 6294: 6156:"Tissue-Specific Features of Innate Lymphoid Cells" 5730: 5299: 5101: 4719: 4475:Lechner MG, Liebertz DJ, Epstein AL (August 2010). 4376: 3816: 3814: 3812: 3810: 3808: 3806: 3804: 3802: 3800: 3798: 3796: 3794: 3792: 3174: 3172: 3170: 3168: 3166: 3164: 3162: 2716: 2675: 2257: 1896: 1894: 1607:ILC2s have also been identified in human and mouse 172:Intracellular microbes (virus, bacteria, parasite) 50:, absence of rearranged antigen receptors found on 6099: 5898: 5889: 5630: 4991: 4824: 3900: 3790: 3788: 3786: 3784: 3782: 3780: 3778: 3776: 3774: 3772: 3523:Palm NW, Rosenstein RK, Medzhitov R (April 2012). 3317: 3076:Mebius RE, Rennert P, Weissman IL (October 1997). 2751: 2096: 2094: 2092: 2090: 2088: 2086: 2084: 2082: 2080: 2078: 2076: 2074: 2072: 1892: 1890: 1888: 1886: 1884: 1882: 1880: 1878: 1876: 1874: 1322:ILC2s support a type- 2 immune environment in the 1262:, and IFN-γ upregulates the prosurvival molecules 905: 637:for their development, activating the fundamental 6144: 5996: 5948: 5946: 5944: 5248: 4946: 4779: 4775: 4773: 4771: 4237: 4235: 4199: 4197: 4195: 4193: 4191: 3675: 3630: 3573: 3466: 3409: 3318:Bando JK, Liang HE, Locksley RM (February 2015). 3313: 3311: 3228: 3226: 2961: 2917: 2857: 2814: 2321: 2319: 2317: 2315: 2313: 2311: 2070: 2068: 2066: 2064: 2062: 2060: 2058: 2056: 2054: 2052: 62:gene), and phenotypic markers usually present on 6787: 6239: 4203: 4055: 4053: 3159: 2370: 882:Identification of the ILC progenitor cell (ILCP) 709:ILC3s are dependent on the transcription factor 690:. Human adult ILC3s, are primarily found in the 5793: 5048: 3857: 3769: 3267: 2722: 2421: 1998: 1996: 1871: 341:, antimicrobial peptides, epithelium survival) 285:production, alternative macrophage activation, 5990: 5941: 5604:The Journal of Allergy and Clinical Immunology 5293: 4768: 4333: 4232: 4188: 3949: 3624: 3460: 3308: 3223: 3069: 3030: 3028: 3026: 3024: 3022: 3020: 3018: 2808: 2471: 2469: 2467: 2465: 2308: 2204: 2049: 1163:LTi cells are present in Peyer’s patches, and 500:in mice, and NK cell receptors (NCRs) such as 477:effect to eradicate intracellular infections. 6431: 5844: 5400:Kondo H, Ichikawa Y, Imokawa G (March 1998). 4050: 3718: 3415: 2872: 1952: 1950: 1822: 1127:, which through the neuroregulatory receptor 26:) are the most recently discovered family of 5787: 5148: 5042: 4241: 4137: 3518: 3516: 3514: 3360: 1993: 1900: 6093: 5899:Sonnenberg GF, Hepworth MR (October 2019). 5838: 5557: 5496: 5494: 5151:"Innate Lymphoid Cells in Mucosal Immunity" 4786:International Journal of Molecular Sciences 4675:Ducimetière L, Vermeer M, Tugues S (2019). 3110: 3015: 2462: 1903:"Innate Lymphoid Cells in Mucosal Immunity" 1791: 1568: 6438: 6424: 5681: 5442: 4940: 4780:Ochel A, Tiegs G, Neumann K (April 2019). 2264:Simonetta F, Pradier A, Roosnek E (2016). 1947: 1750:Historically, the distinction between the 1037:, which activate ILC2s via the release of 722:, depending on the environmental stimuli. 406:Formation of secondary lymphoid structures 6411:Innate Lymphoid Cells in Mucosal Immunity 6271: 6171: 6127: 6117: 6076: 6032: 6022: 5997:Cella M, Otero K, Colonna M (June 2010). 5924: 5872: 5862: 5821: 5811: 5770: 5713: 5534: 5474: 5417: 5376: 5357:Allergy, Asthma & Immunology Research 5327: 5317: 5276: 5266: 5217: 5176: 5166: 5125: 5084: 5074: 5025: 5015: 4974: 4964: 4923: 4863: 4853: 4807: 4797: 4751: 4702: 4692: 4651: 4641: 4600: 4559: 4500: 4451: 4310: 4171: 4161: 4085: 4033: 3924: 3752: 3742: 3724: 3658: 3648: 3607: 3597: 3556: 3511: 3494: 3484: 3443: 3433: 3392: 3343: 3291: 3250: 3206: 3196: 3142: 3093: 3052: 2998: 2988: 2900: 2890: 2840: 2791: 2699: 2658: 2601: 2552: 2503: 2493: 2445: 2404: 2394: 2353: 2343: 2291: 2281: 2240: 2230: 2179: 2120: 1930: 1920: 1846: 1180: 298:Extracellular microbes (bacteria, fungi) 6331: 5491: 5249:Domingues RG, Hepworth MR (2020-02-06). 3119:"The LTi cell, an immunologic chameleon" 1690: 1641: 1633: 1532: 1497: 1436: 1379: 1337: 1240: 1167:, interacting with B cells facilitating 1071: 1019: 864: 810:, and IL-22. They are mediated by RANK, 741: 374: 311: 250: 189: 6678: 3116: 3034: 2475: 1516:aspirin exacerbated respiratory disease 1236: 1080:ILC3s directly interact with bacterial 1061:, and the receptor CCR9. ILC2s express 945: 653: 517:specific function theory. For example, 6788: 6337: 3467:Löser S, Smith KA, Maizels RM (2019). 1104:, and therefore play a role in T cell 798:, however, no NCRs. The expression of 6419: 4885: 4883: 4123:10.1146/annurev-immunol-042617-053238 1808:10.1146/annurev-immunol-020711-075053 1745: 1728:the mechanism is not understood yet. 1709:ILC3s to convert into ILC1-like cells 1702:chronic obstructive pulmonary disease 1669: 1468: 1418: 851:common cytokine- receptor gamma chain 525:, a fundamental feature of NK cells. 5202:"Innate Lymphoid Cells: 10 Years On" 5004:The Journal of Experimental Medicine 2977:The Journal of Experimental Medicine 2218:The Journal of Experimental Medicine 2103:"Innate Lymphoid Cells: 10 Years On" 1614: 1493: 1092:. 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In mice, ILC2s express 528:Due to the production of 488:There are differences in 6173:10.1016/j.it.2020.08.009 6119:10.4049/jimmunol.1601421 5369:10.4168/aair.2011.3.2.81 5268:10.3389/fimmu.2020.00116 5168:10.3389/fimmu.2019.00861 4694:10.3389/fimmu.2019.02895 4602:10.4049/jimmunol.1101270 4534:Zhu J (September 2015). 4493:10.4049/jimmunol.1000901 4256:10.1016/j.it.2019.03.004 3744:10.3389/fimmu.2019.02010 3525:"Allergic host defences" 3486:10.3389/fimmu.2019.00620 2892:10.3389/fimmu.2019.00676 2447:10.4049/jimmunol.1303469 2345:10.3389/fimmu.2019.01192 2283:10.3389/fimmu.2016.00241 1922:10.3389/fimmu.2019.00861 1569:Liver cancer and obesity 1484:type I diabetes mellitus 1306:AhR transcription factor 1115:ILC3s interact with the 1102:co-stimulatory molecules 600:receptors for chemokines 146:Immune function of ILCs 58:(due to the lack of the 6765:Hematopoietic stem cell 6524:Lymphoplasmacytoid cell 6024:10.1073/pnas.1005641107 5527:10.1126/science.1198687 5255:Frontiers in Immunology 5155:Frontiers in Immunology 5076:10.1126/science.aam5809 4681:Frontiers in Immunology 4150:Cell Host & Microbe 4078:10.1126/science.1254009 3731:Frontiers in Immunology 3650:10.1126/science.aan8546 3473:Frontiers in Immunology 3198:10.1126/science.aaa6566 3035:Withers DR (May 2011). 2879:Frontiers in Immunology 2476:Colonna M (June 2018). 2332:Frontiers in Immunology 2270:Frontiers in Immunology 1908:Frontiers in Immunology 1514:, and in patients with 1304:metabolites causes the 1203:, dendritic cells, and 894:transcription factors ( 6297:Seminars in Immunology 4377:Smyth MJ, Godfrey DI, 1756:adaptive immune system 1697: 1647: 1639: 1538: 1503: 1442: 1385: 1246: 1181:Tumor microenvironment 1117:enteric nervous system 1077: 1025: 870: 747: 656:. nILC2s express more 538:cytotoxic CD8+ T cells 469:and other mononuclear 379: 316: 255: 194: 6671:Innate lymphoid cells 6647:Natural killer T cell 6106:Journal of Immunology 5127:10.1093/infdis/jiu106 4732:Nature Communications 4589:Journal of Immunology 4481:Journal of Immunology 2434:Journal of Immunology 1694: 1645: 1637: 1536: 1501: 1440: 1383: 1338:Respiratory infection 1315:Citrobacter rodentium 1244: 1100:receptors, ILCs lack 1075: 1023: 868: 745: 639:transcription factors 424:transcription factors 378: 315: 254: 219:Macrophage activation 193: 20:Innate lymphoid cells 6160:Trends in Immunology 5017:10.1084/jem.20130071 4799:10.3390/ijms20081896 4244:Trends in Immunology 3725:Willinger T (2019). 2990:10.1084/jem.20072713 2232:10.1084/jem.20131560 1769:Innate immune system 1609:white adipose tissue 1237:Liver and metabolism 1125:neurotrophic factors 1035:neuroendocrine cells 946:Origin and migration 814:, IL-17, and IL-22. 293:, thermoregulation) 287:extracellular matrix 36:signalling molecules 30:cells, derived from 6639:Innate-like T cells 6519:Transitional B cell 6015:2010PNAS..10710961C 5857:(41): 70431–70440. 5813:10.1155/2014/923135 5763:10.1038/nature11465 5755:2012Natur.491..254G 5659:10.1038/nature04808 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6131: 6121: 6112:(5): 1798–1803. 6097: 6091: 6090: 6080: 6056: 6047: 6046: 6036: 6026: 5994: 5988: 5987: 5950: 5939: 5938: 5928: 5896: 5887: 5886: 5876: 5866: 5842: 5836: 5835: 5825: 5815: 5791: 5785: 5784: 5774: 5734: 5728: 5727: 5717: 5685: 5679: 5678: 5634: 5628: 5627: 5598: 5592: 5591: 5555: 5549: 5548: 5538: 5498: 5489: 5488: 5478: 5446: 5440: 5439: 5421: 5397: 5391: 5390: 5380: 5348: 5342: 5341: 5331: 5321: 5297: 5291: 5290: 5280: 5270: 5246: 5240: 5239: 5221: 5212:(5): 1054–1066. 5197: 5191: 5190: 5180: 5170: 5146: 5140: 5139: 5129: 5105: 5099: 5098: 5088: 5078: 5046: 5040: 5039: 5029: 5019: 4995: 4989: 4988: 4978: 4968: 4944: 4938: 4937: 4927: 4887: 4878: 4877: 4867: 4857: 4848:(1): 96–108.e9. 4833: 4822: 4821: 4811: 4801: 4777: 4766: 4765: 4755: 4723: 4717: 4716: 4706: 4696: 4672: 4666: 4665: 4655: 4645: 4621: 4615: 4614: 4604: 4580: 4574: 4573: 4563: 4531: 4525: 4521: 4515: 4514: 4504: 4472: 4466: 4465: 4455: 4423: 4417: 4416: 4374: 4368: 4367: 4348:10.1038/35095564 4331: 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2488:(6): 1104–1117. 2473: 2460: 2459: 2449: 2425: 2419: 2418: 2408: 2398: 2374: 2368: 2367: 2357: 2347: 2323: 2306: 2305: 2295: 2285: 2261: 2255: 2254: 2244: 2234: 2208: 2202: 2201: 2183: 2151:Nature Materials 2141: 2135: 2134: 2124: 2115:(5): 1054–1066. 2098: 2047: 2046: 2000: 1991: 1990: 1954: 1945: 1944: 1934: 1924: 1898: 1869: 1868: 1850: 1826: 1820: 1819: 1789: 1311:gastrointestinal 1139:2, which allows 289:/tissue repair, 202: 163:Immune Function 148: 144: 140:circadian rhythm 6816: 6815: 6811: 6810: 6809: 6807: 6806: 6805: 6786: 6785: 6784: 6779: 6747: 6712: 6661: 6633: 6627: 6619: 6611: 6603: 6579: 6571: 6564: 6528: 6506: 6449: 6444: 6387: 6382: 6359:10.1038/nri3389 6342: 6336: 6332: 6293: 6289: 6264:10.1038/ni.3809 6258:(9): 995–1003. 6244: 6240: 6217:10.1038/ni.3800 6201: 6197: 6166:(10): 902–917. 6152: 6145: 6098: 6094: 6057: 6050: 6009:(24): 10961–6. 5995: 5991: 5968:10.1038/ni.3444 5951: 5942: 5911:(10): 599–613. 5897: 5890: 5843: 5839: 5792: 5788: 5749:(7423): 254–8. 5735: 5731: 5706:10.1038/nm.2015 5694:Nature Medicine 5686: 5682: 5645:(7101): 461–5. 5635: 5631: 5599: 5595: 5556: 5552: 5499: 5492: 5467:10.1038/nm.3423 5455:Nature Medicine 5447: 5443: 5398: 5394: 5349: 5345: 5298: 5294: 5247: 5243: 5198: 5194: 5147: 5143: 5106: 5102: 5047: 5043: 5010:(13): 2951–65. 4996: 4992: 4953:Cell Metabolism 4945: 4941: 4902:(7542): 242–6. 4888: 4881: 4834: 4825: 4778: 4769: 4724: 4720: 4673: 4669: 4622: 4618: 4581: 4577: 4532: 4528: 4522: 4518: 4473: 4469: 4424: 4420: 4375: 4371: 4332: 4328: 4283: 4279: 4240: 4233: 4202: 4189: 4142: 4138: 4107: 4103: 4058: 4051: 3998: 3994: 3954: 3950: 3905: 3901: 3866:Nature Medicine 3862: 3858: 3829:(11): 665–678. 3819: 3770: 3723: 3719: 3696:10.1038/ni.2534 3680: 3676: 3629: 3625: 3578: 3574: 3521: 3512: 3465: 3461: 3414: 3410: 3385:10.1038/ni.2187 3365: 3361: 3336:10.1038/ni.3057 3316: 3309: 3286:(12): 2043–54. 3272: 3268: 3231: 3224: 3177: 3160: 3115: 3111: 3074: 3070: 3041:Current Biology 3033: 3016: 2969: 2962: 2939:10.1038/ni.1668 2922: 2918: 2871: 2858: 2833:10.1038/nri3707 2813: 2809: 2756: 2752: 2721: 2717: 2680: 2676: 2623: 2619: 2594:10.1038/ni.2584 2574: 2570: 2525: 2521: 2474: 2463: 2440:(10): 4487–91. 2426: 2422: 2375: 2371: 2324: 2309: 2262: 2258: 2209: 2205: 2142: 2138: 2099: 2050: 2013:(7436): 261–5. 2001: 1994: 1971:10.1038/nri3349 1955: 1948: 1899: 1872: 1848:10.1038/nri3365 1827: 1823: 1790: 1786: 1782: 1765: 1748: 1707:The ability of 1681: 1672: 1663: 1617: 1571: 1551:Crohn’s disease 1543:pathophysiology 1531: 1496: 1471: 1435: 1430: 1421: 1412: 1403: 1397:wound healing. 1378: 1340: 1239: 1183: 1055: 997: 980: 948: 908: 884: 863: 844:differentiation 835: 765:TNF superfamily 757:Peyer’s patches 740: 684: 678: 596:surface markers 556: 550: 479:Oxygen radicals 473:, to induce an 434:-infected, and 416: 227:oxygen radicals 215:Type 1 immunity 200: 154:Tissue Signals 128: 68:dendritic cells 17: 12: 11: 5: 6814: 6804: 6803: 6798: 6781: 6780: 6778: 6777: 6772: 6767: 6761: 6759: 6753: 6752: 6749: 6748: 6746: 6745: 6740: 6735: 6734: 6733: 6723: 6717: 6714: 6713: 6711: 6710: 6705: 6700: 6695: 6690: 6684: 6682: 6673: 6667: 6666: 6663: 6662: 6660: 6659: 6654: 6649: 6643: 6641: 6635: 6634: 6632: 6631: 6630: 6629: 6625: 6621: 6617: 6613: 6609: 6605: 6601: 6592: 6587: 6577: 6569: 6562: 6554: 6548: 6542: 6536: 6530: 6529: 6527: 6526: 6521: 6516: 6515: 6514: 6504: 6500: 6495: 6490: 6485: 6480: 6475: 6470: 6465: 6459: 6457: 6451: 6450: 6443: 6442: 6435: 6428: 6420: 6414: 6413: 6408: 6403: 6398: 6393: 6386: 6385:External links 6383: 6381: 6380: 6330: 6287: 6238: 6195: 6143: 6092: 6048: 5989: 5940: 5888: 5837: 5786: 5729: 5700:(9): 1016–22. 5680: 5629: 5593: 5550: 5513:(6013): 44–9. 5490: 5441: 5392: 5343: 5292: 5241: 5192: 5141: 5120:(3): 493–503. 5100: 5041: 4990: 4939: 4879: 4823: 4767: 4718: 4667: 4616: 4575: 4526: 4516: 4487:(4): 2273–84. 4467: 4418: 4369: 4326: 4277: 4250:(5): 415–430. 4231: 4212:(5): 326–335. 4187: 4136: 4117:(1): 359–381. 4101: 4049: 3992: 3971:10.1038/ni1488 3948: 3919:(6): 1121–33. 3899: 3878:10.1038/nm1720 3856: 3768: 3717: 3674: 3623: 3572: 3510: 3459: 3408: 3359: 3307: 3266: 3245:(2): 340–356. 3222: 3158: 3109: 3088:(4): 493–504. 3068: 3047:(10): R381-2. 3014: 2960: 2916: 2856: 2827:(9): 585–600. 2807: 2750: 2715: 2674: 2617: 2568: 2519: 2461: 2420: 2369: 2307: 2256: 2203: 2158:(2): 250–259. 2136: 2048: 1992: 1946: 1870: 1821: 1783: 1781: 1778: 1777: 1776: 1771: 1764: 1761: 1747: 1744: 1685:classification 1680: 1677: 1671: 1668: 1662: 1659: 1616: 1613: 1570: 1567: 1530: 1527: 1512:rhinosinusitis 1495: 1492: 1470: 1467: 1434: 1431: 1429: 1426: 1420: 1417: 1411: 1408: 1402: 1399: 1377: 1374: 1342:ILC2s promote 1339: 1336: 1324:adipose tissue 1238: 1235: 1201:M1 macrophages 1182: 1179: 1169:IgA production 1054: 1051: 996: 993: 979: 976: 947: 944: 907: 904: 883: 880: 862: 859: 834: 831: 739: 736: 692:lamina propria 680:Main article: 677: 674: 664:, and reduced 633:ILC2s require 552:Main article: 549: 546: 542:T helper cells 415: 412: 409: 408: 403: 381: 372: 359: 343: 342: 335: 318: 309: 299: 295: 294: 279: 257: 248: 235: 231: 230: 212: 196: 187: 174: 165: 164: 161: 158: 155: 152: 127: 126:Classification 124: 15: 9: 6: 4: 3: 2: 6813: 6802: 6801:Immune system 6799: 6797: 6794: 6793: 6791: 6776: 6775:Prolymphocyte 6773: 6771: 6768: 6766: 6763: 6762: 6760: 6758: 6757:Lymphopoiesis 6754: 6744: 6741: 6739: 6736: 6732: 6729: 6728: 6727: 6724: 6722: 6719: 6718: 6715: 6709: 6706: 6704: 6701: 6699: 6696: 6694: 6691: 6689: 6686: 6685: 6683: 6681: 6677: 6674: 6672: 6668: 6658: 6655: 6653: 6650: 6648: 6645: 6644: 6642: 6640: 6636: 6628: 6622: 6620: 6614: 6612: 6606: 6604: 6598: 6597: 6596: 6595:Memory T cell 6593: 6591: 6588: 6585: 6581: 6573: 6565: 6558: 6555: 6553: 6552:Cytotoxic CD8 6549: 6547: 6544: 6543: 6540: 6537: 6535: 6531: 6525: 6522: 6520: 6517: 6513: 6510: 6509: 6508: 6501: 6499: 6496: 6494: 6491: 6489: 6488:Marginal zone 6486: 6484: 6481: 6479: 6476: 6474: 6471: 6469: 6466: 6464: 6461: 6460: 6458: 6456: 6452: 6448: 6441: 6436: 6434: 6429: 6427: 6422: 6421: 6418: 6412: 6409: 6407: 6404: 6402: 6399: 6397: 6394: 6392: 6389: 6388: 6376: 6372: 6368: 6364: 6360: 6356: 6352: 6348: 6341: 6334: 6326: 6322: 6318: 6314: 6310: 6306: 6302: 6298: 6291: 6283: 6279: 6274: 6269: 6265: 6261: 6257: 6253: 6249: 6242: 6234: 6230: 6226: 6222: 6218: 6214: 6210: 6206: 6199: 6191: 6187: 6183: 6179: 6174: 6169: 6165: 6161: 6157: 6150: 6148: 6139: 6135: 6130: 6125: 6120: 6115: 6111: 6107: 6103: 6096: 6088: 6084: 6079: 6074: 6071:(1): 146–60. 6070: 6066: 6062: 6055: 6053: 6044: 6040: 6035: 6030: 6025: 6020: 6016: 6012: 6008: 6004: 6000: 5993: 5985: 5981: 5977: 5973: 5969: 5965: 5962:(6): 636–45. 5961: 5957: 5949: 5947: 5945: 5936: 5932: 5927: 5922: 5918: 5914: 5910: 5906: 5902: 5895: 5893: 5884: 5880: 5875: 5870: 5865: 5860: 5856: 5852: 5848: 5841: 5833: 5829: 5824: 5819: 5814: 5809: 5805: 5801: 5797: 5790: 5782: 5778: 5773: 5768: 5764: 5760: 5756: 5752: 5748: 5744: 5740: 5733: 5725: 5721: 5716: 5711: 5707: 5703: 5699: 5695: 5691: 5684: 5676: 5672: 5668: 5664: 5660: 5656: 5652: 5648: 5644: 5640: 5633: 5625: 5621: 5617: 5613: 5610:(2): 479–85. 5609: 5605: 5597: 5589: 5585: 5581: 5577: 5573: 5569: 5565: 5561: 5554: 5546: 5542: 5537: 5532: 5528: 5524: 5520: 5516: 5512: 5508: 5504: 5497: 5495: 5486: 5482: 5477: 5472: 5468: 5464: 5460: 5456: 5452: 5445: 5437: 5433: 5429: 5425: 5420: 5415: 5412:(3): 769–79. 5411: 5407: 5403: 5396: 5388: 5384: 5379: 5374: 5370: 5366: 5362: 5358: 5354: 5347: 5339: 5335: 5330: 5325: 5320: 5315: 5312:(3): 425–35. 5311: 5307: 5303: 5296: 5288: 5284: 5279: 5274: 5269: 5264: 5260: 5256: 5252: 5245: 5237: 5233: 5229: 5225: 5220: 5215: 5211: 5207: 5203: 5196: 5188: 5184: 5179: 5174: 5169: 5164: 5160: 5156: 5152: 5145: 5137: 5133: 5128: 5123: 5119: 5115: 5111: 5104: 5096: 5092: 5087: 5082: 5077: 5072: 5068: 5064: 5060: 5056: 5052: 5045: 5037: 5033: 5028: 5023: 5018: 5013: 5009: 5005: 5001: 4994: 4986: 4982: 4977: 4972: 4967: 4962: 4959:(4): 685–98. 4958: 4954: 4950: 4943: 4935: 4931: 4926: 4921: 4917: 4913: 4909: 4905: 4901: 4897: 4893: 4886: 4884: 4875: 4871: 4866: 4861: 4856: 4851: 4847: 4843: 4839: 4832: 4830: 4828: 4819: 4815: 4810: 4805: 4800: 4795: 4791: 4787: 4783: 4776: 4774: 4772: 4763: 4759: 4754: 4749: 4745: 4741: 4737: 4733: 4729: 4722: 4714: 4710: 4705: 4700: 4695: 4690: 4686: 4682: 4678: 4671: 4663: 4659: 4654: 4653:11250/2763785 4649: 4644: 4639: 4635: 4631: 4627: 4620: 4612: 4608: 4603: 4598: 4595:(2): 703–13. 4594: 4590: 4586: 4579: 4571: 4567: 4562: 4557: 4553: 4549: 4545: 4541: 4537: 4530: 4520: 4512: 4508: 4503: 4498: 4494: 4490: 4486: 4482: 4478: 4471: 4463: 4459: 4454: 4449: 4445: 4441: 4438:(4): 769–81. 4437: 4433: 4429: 4422: 4414: 4410: 4406: 4402: 4398: 4397:10.1038/86297 4394: 4390: 4386: 4385: 4380: 4373: 4365: 4361: 4357: 4353: 4349: 4345: 4341: 4337: 4330: 4322: 4318: 4313: 4308: 4304: 4300: 4297:(3): 365–77. 4296: 4292: 4288: 4281: 4273: 4269: 4265: 4261: 4257: 4253: 4249: 4245: 4238: 4236: 4227: 4223: 4219: 4215: 4211: 4207: 4200: 4198: 4196: 4194: 4192: 4183: 4179: 4174: 4169: 4164: 4159: 4155: 4151: 4147: 4140: 4132: 4128: 4124: 4120: 4116: 4112: 4105: 4097: 4093: 4088: 4083: 4079: 4075: 4071: 4067: 4063: 4056: 4054: 4045: 4041: 4036: 4031: 4027: 4023: 4019: 4015: 4011: 4007: 4003: 3996: 3988: 3984: 3980: 3976: 3972: 3968: 3965:(9): 967–74. 3964: 3960: 3952: 3944: 3940: 3936: 3932: 3927: 3922: 3918: 3914: 3910: 3903: 3895: 3891: 3887: 3883: 3879: 3875: 3871: 3867: 3860: 3852: 3848: 3844: 3840: 3836: 3832: 3828: 3824: 3817: 3815: 3813: 3811: 3809: 3807: 3805: 3803: 3801: 3799: 3797: 3795: 3793: 3791: 3789: 3787: 3785: 3783: 3781: 3779: 3777: 3775: 3773: 3764: 3760: 3755: 3750: 3745: 3740: 3736: 3732: 3728: 3721: 3713: 3709: 3705: 3701: 3697: 3693: 3689: 3685: 3678: 3670: 3666: 3661: 3656: 3651: 3646: 3642: 3638: 3634: 3627: 3619: 3615: 3610: 3605: 3600: 3595: 3591: 3587: 3583: 3576: 3568: 3564: 3559: 3554: 3550: 3546: 3542: 3538: 3534: 3530: 3526: 3519: 3517: 3515: 3506: 3502: 3497: 3492: 3487: 3482: 3478: 3474: 3470: 3463: 3455: 3451: 3446: 3441: 3436: 3431: 3427: 3423: 3419: 3412: 3404: 3400: 3395: 3390: 3386: 3382: 3379:(2): 144–51. 3378: 3374: 3370: 3363: 3355: 3351: 3346: 3341: 3337: 3333: 3330:(2): 153–60. 3329: 3325: 3321: 3314: 3312: 3303: 3299: 3294: 3289: 3285: 3281: 3277: 3270: 3262: 3258: 3253: 3248: 3244: 3240: 3236: 3229: 3227: 3218: 3214: 3209: 3204: 3199: 3194: 3190: 3186: 3182: 3175: 3173: 3171: 3169: 3167: 3165: 3163: 3154: 3150: 3145: 3140: 3136: 3132: 3128: 3124: 3120: 3113: 3105: 3101: 3096: 3091: 3087: 3083: 3079: 3072: 3064: 3060: 3055: 3050: 3046: 3042: 3038: 3031: 3029: 3027: 3025: 3023: 3021: 3019: 3010: 3006: 3001: 2996: 2991: 2986: 2982: 2978: 2974: 2967: 2965: 2956: 2952: 2948: 2944: 2940: 2936: 2932: 2928: 2920: 2912: 2908: 2903: 2898: 2893: 2888: 2884: 2880: 2876: 2869: 2867: 2865: 2863: 2861: 2852: 2848: 2843: 2838: 2834: 2830: 2826: 2822: 2818: 2811: 2803: 2799: 2794: 2789: 2785: 2781: 2777: 2773: 2769: 2765: 2761: 2754: 2746: 2742: 2738: 2734: 2730: 2726: 2719: 2711: 2707: 2702: 2697: 2694:(4): 649–59. 2693: 2689: 2685: 2678: 2670: 2666: 2661: 2656: 2652: 2648: 2644: 2640: 2636: 2632: 2628: 2621: 2613: 2609: 2604: 2599: 2595: 2591: 2588:(6): 564–73. 2587: 2583: 2579: 2572: 2564: 2560: 2555: 2550: 2546: 2542: 2538: 2534: 2530: 2523: 2515: 2511: 2506: 2501: 2496: 2491: 2487: 2483: 2479: 2472: 2470: 2468: 2466: 2457: 2453: 2448: 2443: 2439: 2435: 2431: 2424: 2416: 2412: 2407: 2402: 2397: 2392: 2388: 2384: 2380: 2373: 2365: 2361: 2356: 2351: 2346: 2341: 2337: 2333: 2329: 2322: 2320: 2318: 2316: 2314: 2312: 2303: 2299: 2294: 2289: 2284: 2279: 2275: 2271: 2267: 2260: 2252: 2248: 2243: 2238: 2233: 2228: 2225:(3): 563–77. 2224: 2220: 2219: 2214: 2207: 2199: 2195: 2191: 2187: 2182: 2177: 2173: 2169: 2165: 2161: 2157: 2153: 2152: 2147: 2140: 2132: 2128: 2123: 2118: 2114: 2110: 2109: 2104: 2097: 2095: 2093: 2091: 2089: 2087: 2085: 2083: 2081: 2079: 2077: 2075: 2073: 2071: 2069: 2067: 2065: 2063: 2061: 2059: 2057: 2055: 2053: 2044: 2040: 2036: 2032: 2028: 2024: 2020: 2016: 2012: 2008: 2007: 1999: 1997: 1988: 1984: 1980: 1976: 1972: 1968: 1964: 1960: 1953: 1951: 1942: 1938: 1933: 1928: 1923: 1918: 1914: 1910: 1909: 1904: 1897: 1895: 1893: 1891: 1889: 1887: 1885: 1883: 1881: 1879: 1877: 1875: 1866: 1862: 1858: 1854: 1849: 1844: 1840: 1836: 1832: 1825: 1817: 1813: 1809: 1805: 1801: 1797: 1796: 1788: 1784: 1775: 1772: 1770: 1767: 1766: 1760: 1757: 1753: 1743: 1740: 1738: 1734: 1729: 1725: 1723: 1717: 1713: 1710: 1705: 1703: 1693: 1689: 1686: 1676: 1667: 1658: 1656: 1652: 1644: 1636: 1632: 1630: 1626: 1622: 1612: 1610: 1605: 1603: 1598: 1594: 1589: 1585: 1579: 1576: 1566: 1562: 1559: 1554: 1552: 1548: 1544: 1535: 1526: 1524: 1519: 1517: 1513: 1509: 1500: 1491: 1487: 1485: 1481: 1477: 1466: 1462: 1458: 1454: 1452: 1448: 1439: 1425: 1416: 1407: 1398: 1396: 1391: 1382: 1373: 1371: 1369: 1368:S. pneumoniae 1363: 1361: 1357: 1352: 1349: 1345: 1335: 1333: 1332:liver disease 1329: 1325: 1320: 1317: 1316: 1312: 1307: 1303: 1298: 1296: 1292: 1288: 1284: 1280: 1276: 1271: 1269: 1265: 1261: 1257: 1253: 1243: 1234: 1231: 1227: 1224: 1220: 1217: 1215: 1211: 1206: 1202: 1197: 1195: 1190: 1186: 1178: 1176: 1175: 1170: 1166: 1161: 1159: 1155: 1150: 1144: 1142: 1138: 1134: 1133:glycosylation 1130: 1126: 1122: 1118: 1113: 1111: 1107: 1103: 1099: 1095: 1091: 1087: 1083: 1074: 1070: 1066: 1064: 1060: 1059:α4β7 integrin 1050: 1046: 1044: 1040: 1036: 1030: 1022: 1018: 1016: 1011: 1009: 1008:smooth muscle 1004: 1002: 992: 988: 984: 975: 973: 969: 968:stromal cells 963: 961: 957: 953: 943: 941: 937: 934:, RORγt, and 933: 929: 925: 921: 917: 913: 903: 901: 897: 893: 889: 879: 876: 867: 858: 856: 852: 847: 845: 841: 830: 828: 824: 820: 815: 813: 809: 805: 801: 797: 793: 789: 785: 781: 777: 773: 772:retinoic acid 768: 766: 762: 758: 754: 744: 735: 733: 729: 723: 721: 716: 712: 707: 705: 701: 697: 693: 689: 683: 673: 671: 667: 663: 659: 655: 649: 647: 643: 640: 636: 631: 629: 625: 621: 617: 613: 609: 605: 601: 597: 592: 590: 586: 582: 578: 574: 570: 566: 562: 555: 545: 543: 539: 535: 531: 526: 524: 520: 515: 511: 507: 503: 499: 494: 491: 486: 484: 480: 476: 475:antimicrobial 472: 468: 464: 460: 456: 452: 448: 443: 441: 437: 433: 429: 425: 421: 407: 404: 402: 401: 397: 393: 389: 385: 382: 377: 373: 371: 370: 367: 363: 360: 357: 353: 349: 348:retinoic acid 345: 344: 340: 336: 334: 333: 330: 326: 322: 319: 314: 310: 308: 307: 303: 300: 297: 296: 292: 288: 284: 280: 278: 277: 273: 269: 265: 261: 258: 253: 249: 247: 246: 243: 239: 236: 233: 232: 228: 224: 220: 216: 213: 211: 210: 207: 203: 197: 192: 188: 186: 185: 182: 178: 175: 173: 170: 167: 166: 162: 159: 156: 153: 150: 149: 143: 141: 137: 136:notch ligands 133: 123: 121: 117: 113: 109: 105: 101: 97: 96:morphogenesis 93: 89: 85: 81: 77: 71: 69: 65: 61: 57: 53: 49: 45: 41: 37: 33: 29: 28:innate immune 25: 21: 6670: 6350: 6346: 6333: 6300: 6296: 6290: 6255: 6251: 6241: 6208: 6204: 6198: 6163: 6159: 6109: 6105: 6095: 6068: 6064: 6006: 6002: 5992: 5959: 5955: 5908: 5904: 5854: 5850: 5840: 5803: 5799: 5789: 5746: 5742: 5732: 5697: 5693: 5683: 5642: 5638: 5632: 5607: 5603: 5596: 5563: 5560:Autoimmunity 5559: 5553: 5510: 5506: 5461:(1): 54–61. 5458: 5454: 5444: 5409: 5405: 5395: 5360: 5356: 5346: 5309: 5305: 5295: 5258: 5254: 5244: 5209: 5205: 5195: 5158: 5154: 5144: 5117: 5113: 5103: 5058: 5054: 5044: 5007: 5003: 4993: 4956: 4952: 4942: 4899: 4895: 4845: 4841: 4789: 4785: 4735: 4731: 4721: 4684: 4680: 4670: 4633: 4630:Cell Reports 4629: 4619: 4592: 4588: 4578: 4546:(1): 14–24. 4543: 4539: 4529: 4524:canimm-0149. 4519: 4484: 4480: 4470: 4435: 4431: 4421: 4391:(4): 293–9. 4388: 4382: 4372: 4339: 4335: 4329: 4294: 4290: 4280: 4247: 4243: 4209: 4205: 4156:(1): 27–37. 4153: 4149: 4139: 4114: 4110: 4104: 4069: 4065: 4009: 4005: 3995: 3962: 3958: 3951: 3916: 3912: 3902: 3872:(3): 282–9. 3869: 3865: 3859: 3826: 3822: 3734: 3730: 3720: 3690:(3): 221–9. 3687: 3683: 3677: 3640: 3636: 3626: 3589: 3585: 3575: 3532: 3528: 3476: 3472: 3462: 3425: 3421: 3411: 3376: 3372: 3362: 3327: 3323: 3283: 3280:Cell Reports 3279: 3269: 3242: 3238: 3188: 3184: 3129:(5): 650–2. 3126: 3122: 3112: 3085: 3081: 3071: 3044: 3040: 2983:(1): 35–41. 2980: 2976: 2933:(1): 66–74. 2930: 2926: 2919: 2882: 2878: 2824: 2820: 2810: 2767: 2763: 2753: 2728: 2724: 2718: 2691: 2687: 2677: 2634: 2630: 2620: 2585: 2581: 2571: 2536: 2532: 2522: 2485: 2481: 2437: 2433: 2423: 2386: 2382: 2372: 2335: 2331: 2273: 2269: 2259: 2222: 2216: 2206: 2155: 2149: 2139: 2112: 2106: 2010: 2004: 1965:(2): 75–87. 1962: 1958: 1912: 1906: 1841:(2): 145–9. 1838: 1834: 1824: 1799: 1793: 1787: 1749: 1741: 1730: 1726: 1721: 1718: 1714: 1706: 1699: 1682: 1673: 1664: 1649: 1618: 1606: 1584:Malnutrition 1580: 1572: 1563: 1555: 1540: 1520: 1508:nasal polyps 1505: 1488: 1472: 1463: 1459: 1455: 1444: 1422: 1413: 1404: 1387: 1367: 1364: 1353: 1341: 1321: 1313: 1299: 1287:liver cancer 1272: 1248: 1228: 1221: 1218: 1198: 1189:Group 1 ILCs 1187: 1184: 1173: 1162: 1145: 1141:fucosylation 1114: 1098:MHC class II 1090:radiotherapy 1086:chemotherapy 1079: 1067: 1056: 1049:and debris. 1047: 1031: 1027: 1012: 1005: 998: 989: 985: 981: 964: 949: 909: 898:, E2-2, and 885: 872: 848: 836: 816: 769: 749: 724: 708: 706:, and skin. 685: 676:Group 3 ILCs 650: 632: 593: 561:amphiregulin 557: 548:Group 2 ILCs 527: 495: 487: 444: 428:cytotoxicity 417: 414:Group 1 ILCs 394: 364: 339:Phagocytosis 327: 304: 291:vasodilation 274: 240: 223:cytotoxicity 204: 179: 171: 129: 114:, bronchial 72: 23: 19: 18: 6796:Lymphocytes 6770:Lymphoblast 6468:Plasmablast 6447:Lymphocytes 6353:(2): 73–4. 5566:(1): 1–14. 5363:(2): 81–8. 4792:(8): 1896. 4738:(1): 8280. 4342:(1): 41–9. 1597:portal vein 1593:fatty acids 1401:Oral mucosa 1376:Skin repair 1348:goblet cell 1275:hepatitis B 1252:hepatocytes 1174:C. dificile 1121:glial cells 952:bone marrow 855:JAK3 kinase 833:Development 761:lymphotoxin 753:lymph nodes 700:endometrium 467:macrophages 392:Lymphotoxin 332:Lymphotoxin 92:homeostasis 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