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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
4
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pubmed:dateCreated |
1996-9-17
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pubmed:abstractText |
Ag-specific activation of T lymphocytes requires two signals, one by the TCR and a second by costimulatory molecules. In a CD4+ T helper cell-dependent experimental autoimmune myocarditis model, we provide genetic evidence that cardiac myosin-induced autoimmune myocarditis and the production of IgG auto-Abs is dependent on functional T cells and did not occur in mice lacking the tyrosine kinase p56lck or the tyrosine phosphatase CD45. By contrast, animals lacking the T cell-costimulatory molecule CD28 (CD28 -/-) developed autoimmune heart disease, although at significantly lower severity than in heterozygous littermates, and produced IgG auto-Abs depending on the concentration of the autoantigen administered. In addition, the isotypes of IgG auto-Abs specific for cardiac myosin differed between CD28 +/- and CD28 -/- mice. Whereas CD28 +/- mice predominantly produced Th2-mediated IgG1 auto-Abs, CD28 -/- mice produced predominantly IgG2a. These data suggest that CD28 costimulation plays a crucial role in induction and maintenance of autoimmune heart disease and that CD28 expression is required for predominant Th2-IgG1 responses in an autoimmune setting.
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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/Antigens, CD28,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD45,
http://linkedlifedata.com/resource/pubmed/chemical/Autoantibodies,
http://linkedlifedata.com/resource/pubmed/chemical/Autoantigens,
http://linkedlifedata.com/resource/pubmed/chemical/Immunoglobulin G,
http://linkedlifedata.com/resource/pubmed/chemical/Immunoglobulin Isotypes,
http://linkedlifedata.com/resource/pubmed/chemical/Lymphocyte Specific Protein...,
http://linkedlifedata.com/resource/pubmed/chemical/Myosins,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Antigen, T-Cell,
http://linkedlifedata.com/resource/pubmed/chemical/src-Family Kinases
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pubmed:status |
MEDLINE
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pubmed:month |
Aug
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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 |
15
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pubmed:volume |
157
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1752-7
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pubmed:dateRevised |
2009-11-19
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pubmed:meshHeading |
pubmed-meshheading:8759765-Animals,
pubmed-meshheading:8759765-Antigens, CD28,
pubmed-meshheading:8759765-Antigens, CD45,
pubmed-meshheading:8759765-Autoantibodies,
pubmed-meshheading:8759765-Autoantigens,
pubmed-meshheading:8759765-Autoimmune Diseases,
pubmed-meshheading:8759765-Immunization,
pubmed-meshheading:8759765-Immunoglobulin G,
pubmed-meshheading:8759765-Immunoglobulin Isotypes,
pubmed-meshheading:8759765-Lymphocyte Specific Protein Tyrosine Kinase p56(lck),
pubmed-meshheading:8759765-Mice,
pubmed-meshheading:8759765-Mice, Knockout,
pubmed-meshheading:8759765-Myocarditis,
pubmed-meshheading:8759765-Myosins,
pubmed-meshheading:8759765-Receptors, Antigen, T-Cell,
pubmed-meshheading:8759765-Signal Transduction,
pubmed-meshheading:8759765-Th2 Cells,
pubmed-meshheading:8759765-src-Family Kinases
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pubmed:year |
1996
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pubmed:articleTitle |
Induction of autoimmunity in the absence of CD28 costimulation.
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pubmed:affiliation |
Amgen Institute, Ontario Cancer Institute, Toronto, Canada.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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