Review
Version 1
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Interleukin-23 Involved in Fibrotic Autoimmune Diseases: New Discoveries
Version 1
: Received: 4 August 2023 / Approved: 7 August 2023 / Online: 7 August 2023 (10:44:21 CEST)
A peer-reviewed article of this Preprint also exists.
Sisto, M.; Lisi, S. Interleukin-23 Involved in Fibrotic Autoimmune Diseases: New Discoveries. J. Clin. Med. 2023, 12, 5699. Sisto, M.; Lisi, S. Interleukin-23 Involved in Fibrotic Autoimmune Diseases: New Discoveries. J. Clin. Med. 2023, 12, 5699.
Abstract
Interleukin (IL)-23 is a central proinflammatory cytokine with a broad range of effects on immune responses. The pathological consequences of excessive IL-23 signaling have been linked to its ability to promote the production of inflammatory mediators such as IL-17, IL-22 by stimulating the differentiation and proliferation of T helper type 17 (Th17 cells). Emerging evidence suggests a potential pro-fibrotic role for IL-23 in the development of chronic inflammatory autoimmune diseases characterized by intense fibrosis. In this review, we summarized the biological features of IL-23 and gathered recent research on the role of IL-23 in fibrotic autoimmune conditions, which could provide a theoretical basis for clinical targeting and drug development.
Keywords
IL-23; autoimmunity; inflammation; fibrosis
Subject
Medicine and Pharmacology, Immunology and Allergy
Copyright: This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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