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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
6
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pubmed:dateCreated |
2000-10-10
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pubmed:abstractText |
The activation of T lymphocytes requires both Ag-mediated signaling through the TCR as well as costimulatory signals transmitted through B7-1 and/or B7-2 with CD28. The interference of B7-mediated costimulatory signals has been proposed as one immunotherapeutic intervention for the prevention autoimmune disease. This study has examined autoantibody responses and autoimmune pathology in a murine model of human systemic lupus erythematosus (SLE), the MRL-lpr/lpr mouse, genetically deficient in B7-1 or B7-2, or in mice treated with B7-1/B7-2 blocking Abs. In contrast to other studies of murine models of SLE, MRL-lpr/lpr mice treated with B7 blocking Abs exhibit strong anti-small nuclear ribonucleoprotein (snRNP) and anti-DNA autoantibody responses with some changes in isotype switching as compared with untreated animals. All MRL-lpr/lpr mice deficient in B7-1 or B7-2 produce anti-snRNP and anti-DNA titers with isotypes virtually identical with wild-type animals. However, the absence of B7-2 costimulation did interfere with the spontaneous activation and the accumulation of memory CD4+ or CD8+ T lymphocytes characteristic of wild-type MRL-lpr/lpr mice. IgG and C3 complement deposition was less pronounced in the kidneys of B7-2 deficient MRL-lpr/lpr mice, reflecting their lessor degree of glomerulonephritis. By comparison, B7-1-deficient MRL-lpr/lpr mice had more severe IgG and C3 deposits in glomeruli.
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pubmed:grant |
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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/Antibodies, Antinuclear,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD80,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD86,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, Differentiation...,
http://linkedlifedata.com/resource/pubmed/chemical/Autoantibodies,
http://linkedlifedata.com/resource/pubmed/chemical/Biological Markers,
http://linkedlifedata.com/resource/pubmed/chemical/Cd86 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Complement C3,
http://linkedlifedata.com/resource/pubmed/chemical/DNA,
http://linkedlifedata.com/resource/pubmed/chemical/Immunoglobulin G,
http://linkedlifedata.com/resource/pubmed/chemical/Immunoglobulin Isotypes,
http://linkedlifedata.com/resource/pubmed/chemical/Immunoglobulin M,
http://linkedlifedata.com/resource/pubmed/chemical/Membrane Glycoproteins,
http://linkedlifedata.com/resource/pubmed/chemical/Ribonucleoproteins, Small Nuclear
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pubmed:status |
MEDLINE
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pubmed:month |
Sep
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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 |
165
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
3436-43
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:10975864-Animals,
pubmed-meshheading:10975864-Antibodies, Antinuclear,
pubmed-meshheading:10975864-Antigens, CD,
pubmed-meshheading:10975864-Antigens, CD80,
pubmed-meshheading:10975864-Antigens, CD86,
pubmed-meshheading:10975864-Antigens, Differentiation, B-Lymphocyte,
pubmed-meshheading:10975864-Autoantibodies,
pubmed-meshheading:10975864-Biological Markers,
pubmed-meshheading:10975864-Complement C3,
pubmed-meshheading:10975864-DNA,
pubmed-meshheading:10975864-Immunoglobulin G,
pubmed-meshheading:10975864-Immunoglobulin Isotypes,
pubmed-meshheading:10975864-Immunoglobulin M,
pubmed-meshheading:10975864-Kidney,
pubmed-meshheading:10975864-Lupus Nephritis,
pubmed-meshheading:10975864-Lymphocyte Activation,
pubmed-meshheading:10975864-Membrane Glycoproteins,
pubmed-meshheading:10975864-Mice,
pubmed-meshheading:10975864-Mice, Inbred BALB C,
pubmed-meshheading:10975864-Mice, Inbred MRL lpr,
pubmed-meshheading:10975864-Mice, Knockout,
pubmed-meshheading:10975864-Ribonucleoproteins, Small Nuclear,
pubmed-meshheading:10975864-T-Lymphocytes
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pubmed:year |
2000
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pubmed:articleTitle |
Autoantibody responses and pathology regulated by B7-1 and B7-2 costimulation in MRL/lpr lupus.
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pubmed:affiliation |
Department of Internal Medicine, Section of Rheumatology, Yale University School of Medicine, New Haven, CT 06510, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.
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