ID: 181. Issue 1 (November 2015)

• Record Type: Journal Article
• Authors: Ouyang, Wenjun
• Is Part Of: Cytokine. Volume 76:Issue 1(2015)
• Page Start: 62
• Publication Date: 2015-11
• Subjects: Cytokines -- Periodicals; 571.844
• DOI: 10.1016/j.cyto.2015.08.029
• Languages: English
• ISSNs: 1043-4666

Abstract

<abstract xml:lang="en" abstract-type="author" id="ab005"> <title> <x xml:space="preserve">Abstract</x> </title> <sec> <p id="sp005">IL-22 is an IL-10 family cytokine, which is predominantly produced by T helper subsets and group 3 innate lymphoid cells (ILCs). IL-22 receptor, IL-22R/IL-10R2, however, is preferentially expressed on tissue epithelial cells such as skin keratinocytes and intestinal epithelial cells. IL-22 induces antimicrobial responses from these epithelial cells. In addition, IL-22 helps to preserve epithelial integrity and promote wound healing responses. We show that IL-22 participates in skin wound healing. In a diabetic wound healing model that mimics the delayed wound healing in diabetic foot ulcer, IL-22 facilitates the healing responses. Similar wound healing response is also observed in the intestine. IL-22 reduces epithelial damage in DSS induced colitis model. Importantly, IL-22 exerts indispensable roles in mucosal immunity. IL-22 can regulate the expression of proinflammatory cytokine, IL-18, in the ileum. IL-18 conversely also promotes IL-22 production from ILCs and Th cells. Interestingly, metabolic disorders compromise mucosal immunity which is associated with reduced IL-22 production. Exogenous IL-22 not only enhances mucosal immunity in diabetic db/db mice, but also improves many metabolic parameters including glucose tolerance and insulin responses.</p> </sec> </abstract>