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dc.contributor.authorSubramanian, Lakshmimathy
dc.contributor.authorBlumenfeld, Hartley
dc.contributor.authorTohn, Robert
dc.contributor.authorLy, Dalam
dc.contributor.authorAguilera, Carlos
dc.contributor.authorMaricic, Igor
dc.contributor.authorMansson, Jan-Eric
dc.contributor.authorBuschard, Karsten
dc.contributor.authorKumar, Vipin
dc.contributor.authorDelovitch, Terry L.
dc.date.accessioned2013-03-11T20:01:04Z
dc.date.issued2012
dc.identifier.citationSubramanian, Lakshmimathy, Hartley Blumenfeld, Robert Tohn, Dalam Ly, Carlos Aguilera, Igor Maricic, Jan-Eric Mansson, Karsten Buschard, Vipin Kumar, and Terry L. Delovitch. 2012. NKT cells stimulated by long fatty acyl chain sulfatides significantly reduces the incidence of type 1 diabetes in nonobese diabetic mice. PLoS ONE 7(5): e37771.en_US
dc.identifier.issn1932-6203en_US
dc.identifier.urihttp://nrs.harvard.edu/urn-3:HUL.InstRepos:10385395
dc.description.abstractSulfatide-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.en_US
dc.language.isoen_USen_US
dc.publisherPublic Library of Scienceen_US
dc.relation.isversionofdoi:10.1371/journal.pone.0037771en_US
dc.relation.hasversionhttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC3359325/pdf/en_US
dash.licenseLAA
dc.subjectBiologyen_US
dc.subjectBiochemistryen_US
dc.subjectLipidsen_US
dc.subjectSphingolipidsen_US
dc.subjectImmunologyen_US
dc.subjectImmune Cellsen_US
dc.subjectT Cellsen_US
dc.subjectImmune Systemen_US
dc.subjectCytokinesen_US
dc.subjectAutoimmunityen_US
dc.subjectImmunomodulationen_US
dc.subjectModel Organismsen_US
dc.subjectAnimal Modelsen_US
dc.subjectMouseen_US
dc.subjectMedicineen_US
dc.subjectEndocrinologyen_US
dc.subjectDiabetic Endocrinologyen_US
dc.subjectDiabetes Mellitus Type 1en_US
dc.titleNKT Cells Stimulated by Long Fatty Acyl Chain Sulfatides Significantly Reduces the Incidence of Type 1 Diabetes in Nonobese Diabetic Miceen_US
dc.typeJournal Articleen_US
dc.description.versionVersion of Recorden_US
dc.relation.journalPLoS ONEen_US
dash.depositing.authorLy, Dalam
dc.date.available2013-03-11T20:01:04Z
dc.identifier.doi10.1371/journal.pone.0037771*
dash.contributor.affiliatedLy, Dalam


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