ArticleDiabetologia2014
IL-17A increases the expression of proinflammatory chemokines in human pancreatic islets.
Article in Diabetologia, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 56 citations in OpenAlex.
- Associations Between Serum Fatty Acids and Immunological Markers in Children Developing Islet Autoimmunity-The TRIGR Nested Case-Control Study.Frontiers in immunology · 2022Trial
- T helper 17 cells and interleukin-17 immunity in type 1 diabetes: From pathophysiology to targeted immunotherapies.World journal of diabetes · 2025Review
- Neutrophils in Type 1 Diabetes: Untangling the Intricate Web of Pathways and Hypothesis.Biomolecules · 2025Review
- Association Between Maternal Mood Disorders and Schizophrenia and the Risk of Type 1 Diabetes in Offspring: A Nationwide Cohort Study.Neuropsychiatric disease and treatment · 2023Article
- Exenatide regulates Th17/Treg balance via PI3K/Akt/FoxO1 pathway in db/db mice.Molecular medicine (Cambridge, Mass.) · 2022Article
- NF-κB-inducing kinase (NIK) is activated in pancreatic β-cells but does not contribute to the development of diabetes.Cell death & disease · 2022Article
- In depth functional characterization of human induced pluripotent stem cell-derived beta cellsFrontiers in cell and developmental biology · 2022Article
- IL-17 is expressed on beta and alpha cells of donors with type 1 and type 2 diabetes.Journal of autoimmunity · 2021Article
- Preventive and therapeutic significance of octreotide combined with lansoprazole on post-ERCP pancreatitis and its effect on serum amylase, inflammatory factors and immune function.Experimental and therapeutic medicine · 2021Article
- IL-17A is involved in diabetic inflammatory pathogenesis by its receptor IL-17RA.Experimental biology and medicine (Maywood, N.J.) · 2021Article
- Good Cop, Bad Cop: The Opposing Effects of Macrophage Activation State on Maintaining or Damaging Functional β-Cell Mass.Metabolites · 2020Review
- IL-17F induces inflammation, dysfunction and cell death in mouse islets.Scientific reports · 2020Article
- Review
- Remission of autoimmune diabetes by anti-TCR combination therapies with anti-IL-17A or/and anti-IL-6 in the IDDM rat model of type 1 diabetes.BMC medicine · 2020Article
- IL-17 in pancreatic disease: pathogenesis and pharmacotherapy.American journal of cancer research · 2020Review
- The miRNAs miR-211-5p and miR-204-5p modulate ER stress in human beta cells.Journal of molecular endocrinology · 2019Article
- The EndoC-βH1 cell line is a valid model of human beta cells and applicable for screenings to identify novel drug target candidates.Molecular metabolism · 2018Article
- Interactions Between the Neuroendocrine System and T Lymphocytes in Diabetes.Frontiers in endocrinology · 2018Review
- Intestinal Immunomodulatory Cells (T Lymphocytes): A Bridge between Gut Microbiota and Diabetes.Mediators of inflammation · 2018Review
- Differential modulation of IL-12 family cytokines in autoimmune islet graft failure in mice.Diabetologia · 2017Article
Corrections and comments
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Authors and funding
13 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aims/hypothesisCytotoxic T cells and macrophages contribute to beta cell destruction in type 1 diabetes at least in part through the production of cytokines such as IL-1β, IFN-γ and TNF-α. We have recently shown the IL-17 pathway to be activated in circulating T cells and pancreatic islets of type 1 diabetes patients. Here, we studied whether IL-17A upregulates the production of chemokines by human pancreatic islets, thus contributing to the build-up of insulitis.
methodsHuman islets (from 18 donors), INS-1E cells and islets from wild-type and Stat1 knockout mice were studied. Dispersed islet cells were left untreated, or were treated with IL-17A alone or together with IL-1β+IFN-γ or TNF-α+IFN-γ. RNA interference was used to knock down signal transducer and activator of transcription 1 (STAT1). Chemokine expression was assessed by quantitative RT-PCR, ELISA and histology. Cell viability was evaluated with nuclear dyes.
resultsIL-17A augmented IL-1β+IFN-γ- and TNF-α+IFN-γ-induced chemokine mRNA and protein expression, and apoptosis in human islets. Beta cells were at least in part the source of chemokine production. Knockdown of STAT1 in human islets prevented cytokine- or IL-17A+cytokine-induced apoptosis and the expression of particular chemokines, e.g. chemokine (C-X-C motif) ligands 9 and 10. Similar observations were made in islets isolated from Stat1 knockout mice. CONCLUSIONS/
interpretationOur findings indicate that IL-17A exacerbates proinflammatory chemokine expression and secretion by human islets exposed to cytokines. This suggests that IL-17A contributes to the pathogenesis of type 1 diabetes by two mechanisms, namely the exacerbation of beta cell apoptosis and increased local production of chemokines, thus potentially aggravating insulitis.
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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.