Innate and Adaptive Interleukin-22 Protects Mice from Inflammatory Bowel Disease

Inflammatory bowel disease (IBD) is a chronic inflammatory disease thought to be mediated by dysfunctional innate and/or adaptive immunity. This aberrant immune response leads to the secretion of harmful cytokines that destroy the epithelium of the gastrointestinal tract and thus cause further infla...

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Veröffentlicht in:Immunity (Cambridge, Mass.) Mass.), 2008-12, Vol.29 (6), p.947-957
Hauptverfasser: Zenewicz, Lauren A., Yancopoulos, George D., Valenzuela, David M., Murphy, Andrew J., Stevens, Sean, Flavell, Richard A.
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Sprache:eng
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Zusammenfassung:Inflammatory bowel disease (IBD) is a chronic inflammatory disease thought to be mediated by dysfunctional innate and/or adaptive immunity. This aberrant immune response leads to the secretion of harmful cytokines that destroy the epithelium of the gastrointestinal tract and thus cause further inflammation. Interleukin-22 (IL-22) is a T helper 17 (Th17) T cell-associated cytokine that is bifunctional in that it has both proinflammatory and protective effects on tissues depending on the inflammatory context. We show herein that IL-22 protected mice from IBD. Interestingly, not only was this protection mediated by CD4 + T cells, but IL-22-expressing natural killer (NK) cells also conferred protection. In addition, IL-22 expression was differentially regulated between NK cell subsets. Thus, both the innate and adaptive immune responses have developed protective mechanisms to counteract the damaging effects of inflammation on tissues.
ISSN:1074-7613
1097-4180
DOI:10.1016/j.immuni.2008.11.003