ArticleFrontiers in immunology2025
IL17-deficient NOD mice are protected from autoimmune diabetes due to decreased antigen presentation and T cell activation.
Article in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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1 citing paper in PubMed.
- Engineered Phytoene-Producing Saccharomyces cerevisiae Alleviates Cyclophosphamide-Induced Intestinal Barrier Dysfunction and Gut Dysbiosis.Probiotics and antimicrobial proteins · 2026Article
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6 authors.
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Abstract
Introduction: IL-17 is a key cytokine helping preserve the intestinal barrier against infections; however, the T cells that primarily secrete IL-17 (Th17) can promote the development of autoimmunity. In Type 1 diabetes, the role of IL-17 is less well understood, with many studies evaluating the role of IL-17, without considering changes within the intestine. Furthermore, therapeutically targeting IL-12/IL-23 (upstream of IL-17) or IL-17 directly can help preserve insulin-producing beta cells in those newly diagnosed with Type 1 diabetes. Thus, there is a need to better understand how IL-17 may modulate susceptibility to Type 1 diabetes by linking intestinal changes to type 1 diabetes development. Methods: We studied IL-17-deficient NOD mice to understand the role of IL-17 in mediatingsusceptibility to Type 1 diabetes in vivo and in vitro. Results: Our study showed that IL-17-deficient NOD mice were protected from autoimmune diabetes, and Discussion: Together, our data suggest a novel role for IL-17 in modulating epithelial cell function and antigen presentation within the intestinal tissue, resulting in reduced autoantigen-specific T cell responses and enhanced protection from autoimmune diabetes. Better understanding of how targeted IL-17 blockade could be administered to the intestine may help better prevent the development of Type 1 diabetes.
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