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• W2001266086 abstract "Group 2 innate lymphoid cells (ILCs) are effector cells shown to function in immunity against helminthic parasites and in tissue repair in lung and intestine. A recent study that appeared in Nature Immunology characterized ILC2 in the skin.1 Dermal ILC2 strongly interact with mast cells and exhibit both pro- and anti-inflammatory activities. ILCs constitute a family of innate lymphocytes distinct from T and B cells and are emerging as important effectors in tissue immunity, homeostasis and (re) modeling. Subsets of ILC have been identified that show remarkable diversity in cytokine production profiles very similar to that of T helper cell subsets. Recently, it has been proposed to classify ILC into three groups, termed group 1, 2 and 3 ILC, based on their cytokine production profile and expression of transcription factors.2, 3 Group 2 ILCs are capable of producing Th2 cytokines interleukin (IL)-5 and IL-13, and like Th2 cells depend on the TF GATA3 for their development, function and maintenance.4 By producing IL-13, ILC2 mediate early immune responses against helminthes. ILC2 by producing IL-5 as well as granulocyte-macrophage colony-stimulating factor mediate recruitment of eosinophils that contribute to the inflammatory response in the lung. ILC2 were also shown to mediate repair of lung tissue damage provoked by viral infection by producing amphiregulin.5 Interestingly, ILC2 are resident in visceral adipose tissue where they are essential for maintenance of eosinophils and alternatively activated macrophages, which are involved in the control of metabolic homeostasis.6 ILC2 also mediate pathology, for instance, by inducing airway hyperreactivity in mouse models for lung inflammation7 and in chronic rhinosinusitis in humans.8 Thus, ILC2 emerge as multitasking cells that are important for immunity against helminthes, tissue repair and homeostasis, but can also go awry and mediate pathology. Papers that appeared in Science Translational Medicine9 and in Nature Immunology1 add another twist to the ILC2 story. Kim et al.9 identified a subset of ILC2 in the skin of mice and show that these cells mediate pathology in mouse models of atopic dermatitis (AD). Skin ILC2 share many features with ILC2 that have been identified in other organs, but Roediger et al.1 show that ILC2 in the skin differ from previously described ILC2 subsets by expression of CD103 and therefore termed these ILC2 as dermal (d) ILC2. dILC2 are radiosensitive cells that like other lymphoid cells depend on the transcription factor Ikaros and are dependent on the IL-7R for their development. Using sophisticated dual-reporter mice with single alleles of IL-4 and IL-13, replaced by AmCyan and dsRed, respectively, Roediger et al.1 demonstrated that ILC2 and not Th2 cells are the major IL-13-producing cells under homeostatic conditions. IL-4 was not expressed by dILC2 under homeostatic conditions, however dILC2 did have the capacity to express IL-4 upon stimulation with TSLP in vivo confirming earlier experiments with human ILC2.4 Thus, both in humans and mice at least a proportion of ILC2 are able to produce IL-4. A question that comes up is whether IL-4-producing ILC2 represents a distinct subset of ILC2 or reflects tight regulation of expression such that only a small proportion expresses IL-4 at any time. It would be highly interesting to determine the function of ILC2-produced IL-4; do they play a role in initiating Th2 cells? Also is there a role of IL4-producing ILC2 in allergic diseases? Using mice with enhanced green fluorescent protein (eGFP) placed in the locus of CCR6, the ILC2 could be visualized as all dILC2 are CCR6 positive and thus expressed eGFP. This permitted analysis of the density of the dILC2 in the skin and their average speed of movement, which revealed that the dILC2 patrol their environment with an average speed similar to that of dermal dendrite cells. Strikingly, analysis of the interactions with other cell types revealed that dILC selectively and strongly interacted with mast cells. As mice with mutations in c-kit showed normal numbers of dILC, the authors conclude that mast cells are not important for dILC2. dILC2, however, may affect the function of mast cells, as IL-13 regulated effector functions of mast cells in vitro. Nevertheless, it was not tested directly in co-culture experiments whether dILC affect mast cell functions. An important question is whether ILC2 also interact directly with mast cells in other organs such as the lung and whether those interactions play important roles in inflammatory reactions in these organs. dILC2 are also present in the skin of Rag−/− mice and depletion of dILC with antibodies against CD90, which in these mice is selectively expressed on ILC, or CD25, which is predominantly but not uniquely expressed on ILC2, would be a way to examine the function of dILC2. Indeed, Kim et al.9 were able to attenuate dILC numbers by antiCD25 treatment and showed that this treatment reduced AD-like pathology by the vitamin D analog MC903. In contrast, Roediger et al.1 did not succeed in achieving depletion of dILC using antibodies. Instead these researchers treated Rag1−/− mice with a complex of IL-2 and the anti-IL-2 antibody JES6-1. Injection of the antibody-IL-2 complex in Rag1−/− mice resulted in a 10-fold expansion of dILC2. These activated cells, which produced IL-5 and IL-13 but not IL-4 and IL-9, were located in close proximity to blood vessels (Figure 1) and showed the same migration behavior as in steady state. In 50% of the IL-2- JES6-1-treated mice skin inflammatory lesions were observed, which showed among others epidermal hyperplasia and eosinophil influx (Figure 1). Whereas eosinophilia is most likely caused by IL-5 secreted by activated dILC2, the skin hyperplasia may be caused by IL-22, which is produced mainly by ILC3. These observations raise the possibility that IL-2-JES6-1 not only activate dILC2, but also ILC3 in the skin. Although this study did not use naked IL-2, the results suggest that IL-2 alone has inflammation-inducing capacity. Where is the IL-2 coming from in wild-type mice? One possibility raised by the authors is that activated T cells are a source (Figure 1), but it has been shown at least in humans that ILC3 are capable of secreting large amounts of IL-2.2 As Roediger's study did not pay attention to other ILC subsets in the skin, study of the roles of ILC2 in conjunction with other ILC subsets in the skin in the steady state and during skin inflammatory diseases will be eagerly waited for. dILC2 present in the dermis are interacting with mast cells. Injection of IL-2 leads to recruitment of dILC2, proliferation and production of IL-5 and IL-13. Whereas IL-5 recruits eosinophils, IL-13 activates mast cells. In a proportion of the IL-2-injected animals this can lead to skin inflammation." @default.
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• W2001266086 date "2013-06-04" @default.
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• W2001266086 title "Group 2 innate lymphoid cells show up in the skin" @default.
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• W2001266086 doi "https://doi.org/10.1038/icb.2013.24" @default.
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