| Literature DB >> 33463541 |
Michael Elias1,2, Shuai Zhao1,2, Hongnga T Le1,2, Jie Wang1,2,3, Markus F Neurath4, Clemens Neufert4, Claudio Fiocchi1,2, Florian Rieder1,2.
Abstract
IL-36 is a member of the IL-1 superfamily and consists of three agonists and one receptor antagonist (IL-36Ra). The three endogenous agonists, IL-36α, -β, and -γ, act primarily as proinflammatory cytokines, and their signaling through the IL-36 receptor (IL-36R) promotes immune cell infiltration and secretion of inflammatory and chemotactic molecules. However, IL-36 signaling also fosters secretion of profibrotic soluble mediators, suggesting a role in fibrotic disorders. IL-36 isoforms and IL-36 have been implicated in inflammatory diseases including psoriasis, arthritis, inflammatory bowel diseases, and allergic rhinitis. Moreover, IL-36 has been connected to fibrotic disorders affecting the kidney, lung, and intestines. This review summarizes the expression, cellular source, and function of IL-36 in inflammation and fibrosis in various organs, and proposes that IL-36 modulation may prove valuable in preventing or treating inflammatory and fibrotic diseases and may reveal a mechanistic link between inflammation and fibrosis.Entities:
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Year: 2021 PMID： 33463541 PMCID： PMC7810483 DOI： 10.1172/JCI144336
Source DB: PubMed Journal: J Clin Invest ISSN： 0021-9738 Impact factor: 14.808