Abstract
Inflammatory bowel diseases (IBD), composed mainly of Crohn's disease (CD) and ulcerative colitis (UC), are strongly implicated in the development of intestinal inflammation lesions. Its exact etiology and pathogenesis are still undetermined. Recently accumulating evidence supports that group 3 innate lymphoid cells (ILC3) are responsible for gastrointestinal mucosal homeostasis through moderate generation of IL-22, IL-17, and GM-CSF in the physiological state. ILC3 contribute to the progression and aggravation of IBD while both IL-22 and IL-17, along with IFN-γ, are overexpressed by the dysregulation of NCR- ILC3 or NCR+ ILC3 function and the bias of NCR+ ILC3 towards ILC1 as well as regulatory ILC dysfunction in the pathological state. Herein, we feature the group 3 innate lymphoid cells' development, biological function, maintenance of gut homeostasis, mediation of IBD occurrence, and potential application to IBD therapy.
Publication types
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Adaptive Immunity
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Animals
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Granulocyte-Macrophage Colony-Stimulating Factor / metabolism
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Homeostasis / immunology
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Humans
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Immunity, Innate
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Inflammation / immunology
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Inflammation / microbiology
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Inflammatory Bowel Diseases / immunology*
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Inflammatory Bowel Diseases / microbiology
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Inflammatory Bowel Diseases / pathology
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Interferon-gamma / metabolism
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Interleukin-17 / metabolism
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Interleukin-22
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Interleukins / metabolism
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Intestinal Mucosa / immunology*
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Intestinal Mucosa / metabolism
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Intestinal Mucosa / microbiology*
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Lymphocytes / immunology*
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Lymphocytes / metabolism
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Lymphocytes / pathology
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Mice
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Natural Cytotoxicity Triggering Receptor 1 / immunology
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Natural Cytotoxicity Triggering Receptor 1 / metabolism
Substances
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Interleukin-17
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Interleukins
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NCR1 protein, human
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Natural Cytotoxicity Triggering Receptor 1
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Interferon-gamma
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Granulocyte-Macrophage Colony-Stimulating Factor