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Molecular role of TGF-beta, secreted from a new type of CD4+ suppressor T cell, NY4.2, in the prevention of autoimmune IDDM in NOD mice.

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dc.contributor.authorHan, HS-
dc.contributor.authorJun, HS-
dc.contributor.authorUtsugi, T-
dc.contributor.authorYoon, JW-
dc.date.accessioned2011-09-27T23:35:57Z-
dc.date.available2011-09-27T23:35:57Z-
dc.date.issued1997-
dc.identifier.issn0896-8411-
dc.identifier.urihttp://repository.ajou.ac.kr/handle/201003/4252-
dc.description.abstractA new type of CD4+ T cell clone (NY4.2) isolated from pancreatic islet-infiltrated lymphocytes of acutely diabetic non-obese diabetic (NOD) mice prevents the development of insulin-dependent diabetes mellitus (IDDM) in NOD mice, as well as the recurrence of autoimmune diabetes in syngeneic islet-transplanted NOD mice. It has been demonstrated that the cytokine TGF-beta, secreted from the cells of this clone, is the substance which prevents autoimmune IDDM. This investigation was initiated to determine the molecular role TGF-beta plays in the prevention of autoimmune IDDM by determining its effect on IL-2-induced signal transduction in Con A-activated NOD mouse splenocytes and HT-2 cells. First, we determined whether TGF-beta, secreted from NY4.2 T cells, inhibits IL-2-dependent T cell proliferation in HT-2 cells (IL-2-dependent T cell line) and NOD splenocytes. We found that TGF-beta suppresses IL-2-dependent T cell proliferation. Second, we determined whether TGF-beta inhibits the activation of Janus kinases (JAKs), as well as signal transducers and activators of transcription (STAT) proteins, involved in an IL-2-induced signalling pathway that normally leads to the proliferation of T cells. We found that TGF-beta inhibited tyrosine phosphorylation of JAK1, JAK3, STAT3 and STAT5 in Con A blasts from NOD splenocytes and HT-2 cells. Third, we examined whether TGF-beta inhibits the cooperation between STAT proteins and mitogen-activated protein kinase (MAPK), especially extracellular signal-regulated kinase 2 (ERK2). We found that TGF-beta inhibited the association of STAT3 and STAT5 with ERK2 in Con A blasts from NOD splenocytes and HT-2 cells. On the basis of these observations, we conclude that TGF-beta may interfere with signal transduction via inhibition of the IL-2-induced JAK/STAT pathway and inhibition of the association of STAT proteins with ERK2 in T cells from NOD splenocytes, resulting in the inhibition of IL-2-dependent T cell proliferation. TGF-beta-mediated suppression of T cell activation may be responsible for the prevention of effector T cell-mediated autoimmune IDDM in NOD mice by TGF-beta-producing CD4+ suppressor T cells.-
dc.language.isoen-
dc.subject.MESHAcute-Phase Proteins-
dc.subject.MESHAnimals-
dc.subject.MESHCD4-Positive T-Lymphocytes-
dc.subject.MESHCalcium-Calmodulin-Dependent Protein Kinases-
dc.subject.MESHCell Line-
dc.subject.MESHDNA-Binding Proteins-
dc.subject.MESHDiabetes Mellitus, Type 1-
dc.subject.MESHDown-Regulation-
dc.subject.MESHEnzyme Activation-
dc.subject.MESHInterleukin-2-
dc.subject.MESHJanus Kinase 1-
dc.subject.MESHJanus Kinase 3-
dc.subject.MESHLymphocyte Activation-
dc.subject.MESHMice-
dc.subject.MESHMice, Inbred NOD-
dc.subject.MESHMilk Proteins-
dc.subject.MESHPhosphorylation-
dc.subject.MESHProtein-Tyrosine Kinases-
dc.subject.MESHReceptors, Interleukin-2-
dc.subject.MESHSTAT3 Transcription Factor-
dc.subject.MESHSTAT5 Transcription Factor-
dc.subject.MESHT-Lymphocytes, Regulatory-
dc.subject.MESHTrans-Activators-
dc.subject.MESHTransforming Growth Factor beta-
dc.titleMolecular role of TGF-beta, secreted from a new type of CD4+ suppressor T cell, NY4.2, in the prevention of autoimmune IDDM in NOD mice.-
dc.typeArticle-
dc.identifier.pmid9218758-
dc.identifier.urlhttp://linkinghub.elsevier.com/retrieve/pii/S0896-8411(97)90137-2-
dc.contributor.affiliatedAuthor윤, 지원-
dc.type.localJournal Papers-
dc.identifier.doi10.1006/jaut.1997.0137-
dc.citation.titleJournal of autoimmunity-
dc.citation.volume10-
dc.citation.number3-
dc.citation.date1997-
dc.citation.startPage299-
dc.citation.endPage307-
dc.identifier.bibliographicCitationJournal of autoimmunity, 10(3). : 299-307, 1997-
dc.identifier.eissn1095-9157-
dc.relation.journalidJ008968411-
Appears in Collections:
Journal Papers > School of Medicine / Graduate School of Medicine > Endocrinology & Metabolism
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