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      The group 2 innate lymphoid cell (ILC2) regulatory network and its underlying mechanisms

      1 , 2 , 3 , 4 , 2 , 5 , 1 , 6
      Immunological Reviews
      Wiley

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          Tuft-cell-derived IL-25 regulates an intestinal ILC2-epithelial response circuit.

          Parasitic helminths and allergens induce a type 2 immune response leading to profound changes in tissue physiology, including hyperplasia of mucus-secreting goblet cells and smooth muscle hypercontractility. This response, known as 'weep and sweep', requires interleukin (IL)-13 production by tissue-resident group 2 innate lymphoid cells (ILC2s) and recruited type 2 helper T cells (TH2 cells). Experiments in mice and humans have demonstrated requirements for the epithelial cytokines IL-33, thymic stromal lymphopoietin (TSLP) and IL-25 in the activation of ILC2s, but the sources and regulation of these signals remain poorly defined. In the small intestine, the epithelium consists of at least five distinct cellular lineages, including the tuft cell, whose function is unclear. Here we show that tuft cells constitutively express IL-25 to sustain ILC2 homeostasis in the resting lamina propria in mice. After helminth infection, tuft-cell-derived IL-25 further activates ILC2s to secrete IL-13, which acts on epithelial crypt progenitors to promote differentiation of tuft and goblet cells, leading to increased frequencies of both. Tuft cells, ILC2s and epithelial progenitors therefore comprise a response circuit that mediates epithelial remodelling associated with type 2 immunity in the small intestine, and perhaps at other mucosal barriers populated by these cells.
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            Human IL-25- and IL-33-responsive type 2 innate lymphoid cells are defined by expression of CRTH2 and CD161.

            Innate lymphoid cells (ILCs) are emerging as a family of effectors and regulators of innate immunity and tissue remodeling. Interleukin 22 (IL-22)- and IL-17-producing ILCs, which depend on the transcription factor RORγt, express CD127 (IL-7 receptor α-chain) and the natural killer cell marker CD161. Here we describe another lineage-negative CD127(+)CD161(+) ILC population found in humans that expressed the chemoattractant receptor CRTH2. These cells responded in vitro to IL-2 plus IL-25 and IL-33 by producing IL-13. CRTH2(+) ILCs were present in fetal and adult lung and gut. In fetal gut, these cells expressed IL-13 but not IL-17 or IL-22. There was enrichment for CRTH2(+) ILCs in nasal polyps of chronic rhinosinusitis, a typical type 2 inflammatory disease. Our data identify a unique type of human ILC that provides an innate source of T helper type 2 (T(H)2) cytokines.
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              Type 2 innate lymphoid cells control eosinophil homeostasis

              Eosinophils are specialized myeloid cells associated with allergy and helminth infections. Blood eosinophils demonstrate circadian cycling, as described over 80 years ago, 1 and are abundant in the healthy gastrointestinal tract. Although a cytokine, interleukin (IL)-5, and chemokines such as eotaxins, mediate eosinophil development and survival, 2 and tissue recruitment, 3 respectively, the processes underlying the basal regulation of these signals remain unknown. Here, we show that serum IL-5 is maintained by long-lived type 2 innate lymphoid cells (ILC2) resident in peripheral tissues. ILC2 secrete IL-5 constitutively and are induced to co-express IL-13 during type 2 inflammation, resulting in localized eotaxin production and eosinophil accumulation. In the small intestine where eosinophils and eotaxin are constitutive, 4 ILC2 co-express IL-5 and IL-13, which is enhanced after caloric intake. The circadian synchronizer vasoactive intestinal peptide (VIP) also stimulates ILC2 through the VPAC2 receptor to release IL-5, linking eosinophil levels with metabolic cycling. Tissue ILC2 regulate basal eosinophilopoiesis and tissue eosinophil accumulation through constitutive and stimulated cytokine expression, and this dissociated regulation can be tuned by nutrient intake and central circadian rhythms.
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                Author and article information

                Journal
                Immunological Reviews
                Immunol Rev
                Wiley
                01052896
                November 2018
                November 2018
                October 07 2018
                : 286
                : 1
                : 37-52
                Affiliations
                [1 ]Laboratory for Immune Cell Systems; RIKEN Center for Integrative Medical Sciences (IMS); Yokohama Japan
                [2 ]Laboratory for Innate Immune Systems; RIKEN Center for Integrative Medical Sciences (IMS); Yokohama Japan
                [3 ]Jill Roberts Institute for Research in Inflammatory Bowel Disease; Joan and Sanford I. Weill Department of Medicine; Department of Microbiology and Immunology; Weill Cornell Medicine; Cornell University; New York New York USA
                [4 ]Division of Pulmonary Medicine; Department of Medicine; Keio University School of Medicine; Tokyo Japan
                [5 ]Division of Immunobiology; Department of Medical Life Science; Graduate School of Medical Life Science; Yokohama City University; Yokohama Japan
                [6 ]Department of Microbiology and Immunology; Keio University School of Medicine; Tokyo Japan
                Article
                10.1111/imr.12706
                30294963
                5bf2c6cb-b455-4014-b438-c4c8f44dc1b1
                © 2018

                http://doi.wiley.com/10.1002/tdm_license_1.1

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