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Citations to this article

IL-36 in chronic inflammation and fibrosis — bridging the gap?
Michael Elias, … , Claudio Fiocchi, Florian Rieder
Michael Elias, … , Claudio Fiocchi, Florian Rieder
Published January 19, 2021
Citation Information: J Clin Invest. 2021;131(2):e144336. https://doi.org/10.1172/JCI144336.
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Review Article has an altmetric score of 15

IL-36 in chronic inflammation and fibrosis — bridging the gap?

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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.

Authors

Michael Elias, Shuai Zhao, Hongnga T. Le, Jie Wang, Markus F. Neurath, Clemens Neufert, Claudio Fiocchi, Florian Rieder

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Total citations by year

Year: 2025 2024 2023 2022 2021 Total
Citations: 6 17 16 15 5 59
Citation information
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