ArticleImmunology2015
Interleukin-17A deficiency ameliorates streptozotocin-induced diabetes.
Article in Immunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 22 citations in OpenAlex.
- Genetically ModifiedJournal of diabetes research · 2026Article
- Diverse functions of myeloid-derived suppressor cells in autoimmune diseases.Immunologic research · 2024Review
- Ginseng-derived panaxadiol ameliorates STZ-induced type 1 diabetes through inhibiting RORγ/IL-17A axis.Acta pharmacologica Sinica · 2023Article
- Interleukin 17A deficiency alleviates neuroinflammation and cognitive impairment in an experimental model of diabetic encephalopathy.Neural regeneration research · 2022Article
- Kidney microRNA Expression Pattern in Type 2 Diabetic Nephropathy in BTBR Ob/Ob Mice.Frontiers in pharmacology · 2022Article
- IL-17A Damages the Blood-Retinal Barrier through Activating the Janus Kinase 1 Pathway.Biomedicines · 2021Article
- IL-17A is involved in diabetic inflammatory pathogenesis by its receptor IL-17RA.Experimental biology and medicine (Maywood, N.J.) · 2021Article
- Emerging Roles of Myeloid-Derived Suppressor Cells in Diabetes.Frontiers in pharmacology · 2021Review
- Metabolic abnormalities exacerbate Sjögren's syndrome by and is associated with increased the population of interleukin-17-producing cells in NOD/ShiLtJ mice.Journal of translational medicine · 2020Article
- Could IL-17A Be a Novel Therapeutic Target in Diabetic Nephropathy?Journal of clinical medicine · 2020Review
- Amelioration of type 1 diabetes by recombinant fructose-1,6-bisphosphate aldolase and cystatin derived from Schistosoma japonicum in a murine model.Parasitology research · 2020Article
- Human Gingiva-Derived Mesenchymal Stem Cells Ameliorate Streptozoticin-induced T1DM in mice via Suppression of T effector cells and Up-regulating Treg Subsets.Scientific reports · 2017Article
- Cholinergic Stimulation Prevents the Development of Autoimmune Diabetes: Evidence for the Modulation of Th17 Effector Cells via an IFNγ-Dependent Mechanism.Frontiers in immunology · 2016Article
- Th17 Cells in Type 1 Diabetes: Role in the Pathogenesis and Regulation by Gut Microbiome.Mediators of inflammation · 2015Review
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Interleukin-17 (IL-17) is a cytokine with critical functions in multiple autoimmune diseases. However, its roles in type I diabetes and the underlying mechanisms remain to be fully elucidated. In the current study, we investigated the impact of IL-17 deficiency on streptozotocin (STZ) -induced diabetes. Il-17(-/-) mice exhibited attenuated hyperglycaemia and insulitis after STZ treatment compared with control mice. The Il-17(-/-) mice had fewer CD8(+) cells infiltrating the pancreas than wild-type controls after STZ injection. Wild-type mice showed increased percentage and number of splenic CD8(+) cells and decreased Gr1(+) CD11b(+) myeloid-derived suppressor cells (MDSC) after STZ treatment, but Il-17(-/-) mice maintained the percentages and numbers of splenic CD8(+) cells and MDSC, suggesting that IL-17 is implicated in STZ-induced cellular immune responses in the spleen. We further purified the MDSC from spleens of STZ-treated mice. Il-17(-/-) MDSC showed increased ability to suppress CD8(+) cell proliferation in vitro compared with wild-type MDSC. Transfer of MDSC to diabetic mice showed that MDSC from Il-17(-/-) mice could ameliorate hyperglycaemia. Moreover, recipients with MDSC from Il-17(-/-) mice had a decreased percentage of CD8(+) cell in the spleen compared with recipients with MDSC from wild-type mice. These data suggest that IL-17 is required in splenic MDSC function after STZ delivery. In summary, our study has revealed a pathogenic role of IL-17 in an STZ-induced diabetes model with important implications for our understanding of IL-17 function in autoimmune diseases.
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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.