| pubmed-article:9218758 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:9218758 | lifeskim:mentions | umls-concept:C0035820 | lld:lifeskim |
| pubmed-article:9218758 | lifeskim:mentions | umls-concept:C0085243 | lld:lifeskim |
| pubmed-article:9218758 | lifeskim:mentions | umls-concept:C0011854 | lld:lifeskim |
| pubmed-article:9218758 | lifeskim:mentions | umls-concept:C0038856 | lld:lifeskim |
| pubmed-article:9218758 | lifeskim:mentions | umls-concept:C1327616 | lld:lifeskim |
| pubmed-article:9218758 | lifeskim:mentions | umls-concept:C0040690 | lld:lifeskim |
| pubmed-article:9218758 | lifeskim:mentions | umls-concept:C0443146 | lld:lifeskim |
| pubmed-article:9218758 | lifeskim:mentions | umls-concept:C1521991 | lld:lifeskim |
| pubmed-article:9218758 | lifeskim:mentions | umls-concept:C1332714 | lld:lifeskim |
| pubmed-article:9218758 | lifeskim:mentions | umls-concept:C1708528 | lld:lifeskim |
| pubmed-article:9218758 | lifeskim:mentions | umls-concept:C1554124 | lld:lifeskim |
| pubmed-article:9218758 | pubmed:issue | 3 | lld:pubmed |
| pubmed-article:9218758 | pubmed:dateCreated | 1997-8-19 | lld:pubmed |
| pubmed-article:9218758 | pubmed:abstractText | A 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. | lld:pubmed |
| pubmed-article:9218758 | pubmed:language | eng | lld:pubmed |
| pubmed-article:9218758 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9218758 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:9218758 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:9218758 | pubmed:month | Jun | lld:pubmed |
| pubmed-article:9218758 | pubmed:issn | 0896-8411 | lld:pubmed |
| pubmed-article:9218758 | pubmed:author | pubmed-author:YoonJ WJW | lld:pubmed |
| pubmed-article:9218758 | pubmed:author | pubmed-author:PanP CPC | lld:pubmed |
| pubmed-article:9218758 | pubmed:author | pubmed-author:LueK YKY | lld:pubmed |
| pubmed-article:9218758 | pubmed:author | pubmed-author:UtsugiTT | lld:pubmed |
| pubmed-article:9218758 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:9218758 | pubmed:volume | 10 | lld:pubmed |
| pubmed-article:9218758 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:9218758 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:9218758 | pubmed:pagination | 299-307 | lld:pubmed |
| pubmed-article:9218758 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
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| pubmed-article:9218758 | pubmed:year | 1997 | lld:pubmed |
| pubmed-article:9218758 | pubmed:articleTitle | 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. | lld:pubmed |
| pubmed-article:9218758 | pubmed:affiliation | Department of Microbiology and Infectious Diseases, Julia McFarlane Diabetes Research Centre, Faculty of Medicine, The University of Calgary, Alberta, Canada. | lld:pubmed |
| pubmed-article:9218758 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:9218758 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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