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Control of autoimmune diabetes in NOD mice by GAD expression or suppression in beta cells.

DC Field Value Language
dc.contributor.authorYoon, JW-
dc.contributor.authorYoon, CS-
dc.contributor.authorLim, HW-
dc.contributor.authorHuang, QQ-
dc.contributor.authorKang, Y-
dc.contributor.authorPyun, KH-
dc.contributor.authorHirasawa, K-
dc.contributor.authorSherwin, RS-
dc.contributor.authorJun, HS-
dc.date.accessioned2011-09-20T05:08:30Z-
dc.date.available2011-09-20T05:08:30Z-
dc.date.issued1999-
dc.identifier.issn0193-4511-
dc.identifier.urihttp://repository.ajou.ac.kr/handle/201003/4225-
dc.description.abstractGlutamic acid decarboxylase (GAD) is a pancreatic beta cell autoantigen in humans and nonobese diabetic (NOD) mice. beta Cell-specific suppression of GAD expression in two lines of antisense GAD transgenic NOD mice prevented autoimmune diabetes, whereas persistent GAD expression in the beta cells in the other four lines of antisense GAD transgenic NOD mice resulted in diabetes, similar to that seen in transgene-negative NOD mice. Complete suppression of beta cell GAD expression blocked the generation of diabetogenic T cells and protected islet grafts from autoimmune injury. Thus, beta cell-specific GAD expression is required for the development of autoimmune diabetes in NOD mice, and modulation of GAD might, therefore, have therapeutic value in type 1 diabetes.-
dc.language.isoen-
dc.subject.MESHAdoptive Transfer-
dc.subject.MESHAnimals-
dc.subject.MESHAutoantigens/genetics-
dc.subject.MESHAutoantigens/immunology*-
dc.subject.MESHAutoantigens/physiology-
dc.subject.MESHAutoimmunity-
dc.subject.MESHDNA, Antisense-
dc.subject.MESHDiabetes Mellitus, Type 1/enzymology*-
dc.subject.MESHDiabetes Mellitus, Type 1/immunology*-
dc.subject.MESHDiabetes Mellitus, Type 1/pathology-
dc.subject.MESHFemale-
dc.subject.MESHGene Expression-
dc.subject.MESHGlutamate Decarboxylase/genetics-
dc.subject.MESHGlutamate Decarboxylase/immunology*-
dc.subject.MESHGlutamate Decarboxylase/physiology-
dc.subject.MESHInsulin/blood-
dc.subject.MESHInsulin/metabolism-
dc.subject.MESHIslets of Langerhans/enzymology*-
dc.subject.MESHIslets of Langerhans/immunology-
dc.subject.MESHIslets of Langerhans/metabolism-
dc.subject.MESHIslets of Langerhans/pathology-
dc.subject.MESHIslets of Langerhans Transplantation-
dc.subject.MESHLymphocyte Activation-
dc.subject.MESHMale-
dc.subject.MESHMice-
dc.subject.MESHMice, Inbred NOD-
dc.subject.MESHMice, SCID-
dc.subject.MESHMice, Transgenic-
dc.subject.MESHT-Lymphocytes/immunology-
dc.subject.MESHTransgenes-
dc.titleControl of autoimmune diabetes in NOD mice by GAD expression or suppression in beta cells.-
dc.typeArticle-
dc.identifier.pmid10325232-
dc.identifier.urlhttp://www.sciencemag.org/cgi/pmidlookup?view=long&pmid=10325232-
dc.contributor.affiliatedAuthor윤, 지원-
dc.contributor.affiliatedAuthor강, 엽-
dc.type.localJournal Papers-
dc.citation.titleScience-
dc.citation.volume284-
dc.citation.number5417-
dc.citation.date1999-
dc.citation.startPage1183-
dc.citation.endPage1187-
dc.identifier.bibliographicCitationScience, 284(5417):1183-1187, 1999-
Appears in Collections:
Journal Papers > School of Medicine / Graduate School of Medicine > Endocrinology & Metabolism
Journal Papers > School of Medicine / Graduate School of Medicine > Physiology
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