IL-36 in chronic inflammation and fibrosis - bridging the gap?
Elias M, Zhao S, Le HT, Wang J, Neurath M, Neufert C, Fiocchi C, Rieder F (2021)
Publication Type: Journal article, Review article
Publication year: 2021
Journal
Book Volume: 131
Article Number: e144336
Journal Issue: 2
DOI: 10.1172/JCI144336
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.
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United States (USA) (US)How to cite
APA:
Elias, M., Zhao, S., Le, H.T., Wang, J., Neurath, M., Neufert, C.,... Rieder, F. (2021). IL-36 in chronic inflammation and fibrosis - bridging the gap? Journal of Clinical Investigation, 131(2). https://doi.org/10.1172/JCI144336
MLA:
Elias, Michael, et al. "IL-36 in chronic inflammation and fibrosis - bridging the gap?" Journal of Clinical Investigation 131.2 (2021).
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