ArticlePloS one2012
NKT cells stimulated by long fatty acyl chain sulfatides significantly reduce the incidence of type 1 diabetes in nonobese diabetic mice [corrected].
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 37 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
37 citing papers in PubMed, 53 citations in OpenAlex.
- Functions of Sulfatide in the Nervous, Immune, and Urinary Systems.Advances in experimental medicine and biology · 2026Review
- A direct effect of sulfatide against development of fibrosis.Metabolism open · 2025Article
- Decrypting the Possible Mechanistic Role of Fenofibrate in Alzheimer's Disease and Type 2 Diabetes: The Truth and Mystery.Journal of cellular and molecular medicine · 2025Review
- NKT Hybridoma Cell Stimulation Assays to Evaluate Glycolipid Specificity and Processing.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Diverse NKT cells regulate early inflammation and neurological outcomes after cardiac arrest and resuscitation.Science translational medicine · 2024Article
- Probiotic treatment with viable α-galactosylceramide-producing Bacteroides fragilis reduces diabetes incidence in female nonobese diabetic mice.Journal of diabetes · 2024Article
- Lysosomal processing of sulfatide analogs alters target NKT cell specificity and immune responses in cancer.The Journal of clinical investigation · 2023Article
- Pancreatic draining lymph nodes (PLNs) serve as a pathogenic hub contributing to the development of type 1 diabetes.Cell & bioscience · 2023Review
- Article
- The etiology and pathogenesis of type 1 diabetes - A personal, non-systematic review of possible causes, and interventions.Frontiers in endocrinology · 2022Review
- Insulin Independence in Newly Diagnosed Type 1 Diabetes Patient following Fenofibrate Treatment.Case reports in medicine · 2020Article
- PPARs and the Development of Type 1 Diabetes.PPAR research · 2020Review
- Fenofibrate increases very-long-chain sphingolipids and improves blood glucose homeostasis in NOD mice.Diabetologia · 2019Article
- Abnormal islet sphingolipid metabolism in type 1 diabetes.Diabetologia · 2018Article
- The Janus Face of NKT Cell Function in Autoimmunity and Infectious Diseases.International journal of molecular sciences · 2018Review
- Type II NKT Cells: An Elusive Population With Immunoregulatory Properties.Frontiers in immunology · 2018Review
- L-serine supplementation lowers diabetes incidence and improves blood glucose homeostasis in NOD mice.PloS one · 2018Article
- Complex Network of NKT Cell Subsets Controls Immune Homeostasis in Liver and Gut.Frontiers in immunology · 2018Review
- Type II NKT Cells and Their Emerging Role in Health and Disease.Journal of immunology (Baltimore, Md. : 1950) · 2017Review
- Type II NKT cells: a distinct CD1d-restricted immune regulatory NKT cell subset.Immunogenetics · 2016Review
Corrections and comments
- Erratum issued
- Erratum issued
Authors and funding
10 authors at 4 institutions in 4 countries.
Funding
Abstract
Sulfatide-reactive type II NKT cells have been shown to regulate autoimmunity and anti-tumor immunity. Although, two major isoforms of sulfatide, C16:0 and C24:0, are enriched in the pancreas, their relative role in autoimmune diabetes is not known. Here, we report that sulfatide/CD1d-tetramer(+) cells accumulate in the draining pancreatic lymph nodes, and that treatment of NOD mice with sulfatide or C24:0 was more efficient than C16:0 in stimulating the NKT cell-mediated transfer of a delay in onset from T1D into NOD.Scid recipients. Using NOD.CD1d(-/-) mice, we show that this delay of T1D is CD1d-dependent. Interestingly, the latter delay or protection from T1D is associated with the enhanced secretion of IL-10 rather than IFN-g by C24:0-treated CD4(+) T cells and the deviation of the islet-reactive diabetogenic T cell response. Both C16:0 and C24:0 sulfatide isoforms are unable to activate and expand type I iNKT cells. Collectively, these data suggest that C24:0 stimulated type II NKT cells may regulate protection from T1D by activating DCs to secrete IL-10 and suppress the activation and expansion of type I iNKT cells and diabetogenic T cells. Our results raise the possibility that C24:0 may be used therapeutically to delay the onset and protect from T1D in humans.
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Registered trials
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.