ArticleScientific reports2020
IL-17F induces inflammation, dysfunction and cell death in mouse islets.
Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 5 citations in OpenAlex.
- Diabetes exacerbates experimental peri-implantitis in mice with elevated IL-17A-associated inflammation and IL-17F upregulation.Scientific reports · 2026Article
- T cells are necessary for development of PCOS reproductive symptoms in a letrozole-induced mouse model of PCOS.bioRxiv : the preprint server for biology · 2025Article
- Inflammation and resolution in obesity.Nature reviews. Endocrinology · 2025 · on this mapReview
- Proteomic Predictors of Incident Diabetes: Results From the Atherosclerosis Risk in Communities (ARIC) Study.Diabetes care · 2023Article
- Production of rAAV by plasmid transfection induces antiviral and inflammatory responses in suspension HEK293 cells.Molecular therapy. Methods & clinical development · 2023Article
- Contribution of Interleukin-17A to Retinal Degenerative Diseases.Frontiers in immunology · 2022Review
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
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Abstract
Type 17 immune responses, typified by the production of the cytokines IL-17A and IL-17F, have been implicated in the development of type 1 diabetes in animal models and human patients, however the underlying pathogenic mechanisms have not been clearly elucidated. While previous studies show that IL-17A enhances inflammatory gene expression and cell death in mouse β-cells and human islets, the function of IL-17F in pancreatic β-cells is completely untested to date. Here we show that IL-17F exhibits potent pathogenic effects in mouse β-cell lines and islets. IL-17F signals via the IL-17RA and -RC subunits in β-cells and in combination with other inflammatory cytokines induces expression of chemokine transcripts, suppresses the expression of β-cell identity genes and impairs glucose stimulated insulin secretion. Further IL-17F induces cell death in primary mouse islets. This occurs via Jnk, p38 and NF-κB dependent induction of Nos2 and is completely ablated in the presence of an inducible nitric oxide synthase (iNOS) inhibitor. Together these data indicate that IL-17F possesses similar pathogenic activities to IL-17A in mouse β-cell lines and islets and is likely to be a type 17 associated pathogenic factor in type 1 diabetes.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.