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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
11
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pubmed:dateCreated |
2001-11-20
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pubmed:abstractText |
BDC2.5/nonobese diabetic (NOD) transgenic mice express a TCR from a diabetogenic T cell clone yet do not spontaneously develop diabetes at high incidence. Evidence exists showing that in the absence of endogenous TCR alpha-chain rearrangements this transgenic mouse spontaneously develops diabetes and that CTLA-4 negatively regulates diabetes onset. This strongly suggests that onset of diabetes in BDC2.5/NOD mice is governed by T cell regulation. We addressed the mechanism of immune regulation in BDC2.5/NOD mice. We find that activated spleen cells from young, but not old, BDC2.5/NOD mice are able to transfer diabetes to NOD-scid recipients. We have used anti-IL-10R to show that the failure of splenocytes from older mice to transfer diabetes is due to dominant regulation. We furthermore found that diabetes developed following anti-IL-10R treatment of 6-wk old BDC2.5/NOD mice indicating that endogenous IL-10 plays a key role in the regulation of diabetes onset in this transgenic mouse.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Cytokines,
http://linkedlifedata.com/resource/pubmed/chemical/Immune Sera,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-10,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Antigen, T-Cell,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Interleukin,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Interleukin-10,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Interleukin-2
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pubmed:status |
MEDLINE
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pubmed:month |
Dec
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pubmed:issn |
0022-1767
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:day |
1
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pubmed:volume |
167
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
6087-91
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:11714766-Adoptive Transfer,
pubmed-meshheading:11714766-Aging,
pubmed-meshheading:11714766-Animals,
pubmed-meshheading:11714766-Antibody Specificity,
pubmed-meshheading:11714766-Cells, Cultured,
pubmed-meshheading:11714766-Cytokines,
pubmed-meshheading:11714766-Diabetes Mellitus, Type 1,
pubmed-meshheading:11714766-Female,
pubmed-meshheading:11714766-Immune Sera,
pubmed-meshheading:11714766-Interleukin-10,
pubmed-meshheading:11714766-Lymphocyte Activation,
pubmed-meshheading:11714766-Male,
pubmed-meshheading:11714766-Mice,
pubmed-meshheading:11714766-Mice, Inbred NOD,
pubmed-meshheading:11714766-Mice, SCID,
pubmed-meshheading:11714766-Mice, Transgenic,
pubmed-meshheading:11714766-Receptors, Antigen, T-Cell,
pubmed-meshheading:11714766-Receptors, Interleukin,
pubmed-meshheading:11714766-Receptors, Interleukin-10,
pubmed-meshheading:11714766-Receptors, Interleukin-2,
pubmed-meshheading:11714766-Spleen
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pubmed:year |
2001
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pubmed:articleTitle |
Cutting edge: interactions through the IL-10 receptor regulate autoimmune diabetes.
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pubmed:affiliation |
Department of Pathology, University of Cambridge, Cambridge, United Kingdom.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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