ArticleJournal of immunology (Baltimore, Md. : 1950)2014
Islet antigen-specific Th17 cells can induce TNF-α-dependent autoimmune diabetes.
Article in Journal of immunology (Baltimore, Md. : 1950), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 49 citations in OpenAlex.
- Ustekinumab for type 1 diabetes in adolescents: a multicenter, double-blind, randomized phase 2 trial.Nature medicine · 2024Trial
- T helper 17 cells and interleukin-17 immunity in type 1 diabetes: From pathophysiology to targeted immunotherapies.World journal of diabetes · 2025Review
- Single-cell analysis reveals islet autoantigen's immune activation in type 1 diabetes patients.Journal of clinical biochemistry and nutrition · 2025Article
- Antidiabetic and Immunoregulatory Activities of Extract ofInternational journal of molecular sciences · 2023Article
- The role of cytokines and T-bet, GATA3, ROR-γt, and FOXP3 transcription factors of T cell subsets in the natural clinical progression of Type 1 Diabetes.Immunologic research · 2023Article
- Ectopic Colonization and Immune Landscapes of Periodontitis Microbiota in Germ-Free Mice With Streptozotocin-Induced Type 1 Diabetes Mellitus.Frontiers in microbiology · 2022Article
- Investigating the Mechanism of Rhizoma Coptidis-Eupatorium fortunei Medicine in the Treatment of Type 2 Diabetes Based on Network Pharmacology and Molecular Docking.BioMed research international · 2022Article
- Altered expression of Tim family molecules and an imbalanced ratio of Tim-3 to Tim-1 expression in patients with type 1 diabetes.Frontiers in endocrinology · 2022Article
- Lymphotoxins Serve as a Novel Orchestrator in T1D Pathogenesis.Frontiers in immunology · 2022Review
- Transgenic Overexpression of Galectin-3 in Pancreatic β Cells Attenuates Hyperglycemia in Mice: Synergistic Antidiabetic Effect With Exogenous IL-33.Frontiers in pharmacology · 2021Article
- Lipid deposition and metaflammation in diabetic kidney disease.Current opinion in pharmacology · 2020Review
- Pathogenic Pathways and Therapeutic Approaches Targeting Inflammation in Diabetic Nephropathy.International journal of molecular sciences · 2020Review
- miR-802 participates in the inflammatory process of inflammatory bowel disease by suppressing SOCS5.Bioscience reports · 2020Article
- Could IL-17A Be a Novel Therapeutic Target in Diabetic Nephropathy?Journal of clinical medicine · 2020Review
- Article
- IL-17 in pancreatic disease: pathogenesis and pharmacotherapy.American journal of cancer research · 2020Review
- Cytokines in type 1 diabetes: mechanisms of action and immunotherapeutic targets.Clinical & translational immunology · 2020Review
- T cells instruct myeloid cells to produce inflammasome-independent IL-1β and cause autoimmunity.Nature immunology · 2020Article
- Downregulation of T-Cell Transcription Factors in Adult Latent Autoimmune Diabetes with High-Titer Glutamic Acid Decaroxylase Antibody.Diabetes therapy : research, treatment and education of diabetes and related disorders · 2019Article
- The Relationship between Epicardial Adipose Tissue Thickness and Serum Interleukin-17a Level in Patients with Isolated Metabolic Syndrome.Biomolecules · 2019Observational
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Type 1 diabetes (T1D) results from autoimmune destruction of pancreatic β-cells. Although Th1 cells are key orchestrators of T1D, the function(s) of the more recently identified Th17 subset are unclear due to inherent plasticity. In this study, we analyzed Th17 cells for stability and diabetogenicity in NOD mice. We found that like Th1 cells, Th17 are a distinct population throughout the prediabetic phase. At diabetes onset, there were marked increases in IL-17-producing Th17 cells and IFN-γ-producing Th1 cells in the pancreas as well as in the serum levels of these cytokines, indicating that these proinflammatory mediators serve as biomarkers of advanced autoimmunity. Although naturally occurring Th17 cells in diabetic mice did not contribute to diabetes development in transfer models, islet-specific Th17 cells were diabetogenic independently of IL-17 and displayed inflammation-induced Th17-to-Th1 reprogramming that could be elicited by Th1 cells. However, an inability to generate Th1 cells because of Stat4, Ifngr, and Ifng deficiencies did not prevent diabetes. Instead, TNF-α could mediate diabetes in response to either Th17 cells or Th1 cells. The results identify a previously unknown mechanism by which Th17 cells can contribute to T1D. Our studies also suggest that when developing interventions for T1D, it will be potentially advantageous to focus on mechanisms common to effector T cells rather than on the signature cytokines of various subsets.
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