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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
1
|
| pubmed:dateCreated |
1987-1-21
|
| pubmed:abstractText |
MRL-lpr/lpr mice spontaneously develop massive T cell lymphadenopathy, autoantibodies, and immune-mediated pathology. These mice are thought to be models of various human autoimmune diseases, including systemic lupus, Sjogren's syndrome, and rheumatoid arthritis. We have used cyclosporin A (CS-A) treatment as a tool by which the mechanisms of immune-mediated pathology might be dissected. CS-A was used because of its known preferential inhibition of T cell function and the marked expansion in MRL-lpr/lpr mice of an unusual L3T4-, Lyt-2-, 6B2+ T cell population. CS-A prevented lymphadenopathy and expansion of L3T4-, Lyt-2-, 6B2+ T cells in the peripheral lymph nodes, and also in the thymus. The increased expression of the c-myb and T cell receptor beta-chain genes associated with these unusual cells was also corrected. The finding of increased numbers of L3T4-, Lyt-2-, 6B2+ thymocytes in untreated mice suggests abnormal intrathymic differentiation in lpr/lpr mice, a defect that was corrected by CS-A. Treated mice had a marked decrease in arthritis and glomerulonephritis and significantly prolonged survival. These beneficial effects of CS-A occurred despite a lack of reduction in antibodies reactive with DNA, circulating immune complexes, rheumatoid factor titers, or immunoglobulin concentrations. These results demonstrate that the B cell hyperactivity of MRL-lpr/lpr mice can proceed without the T cell proliferative disease.
|
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
AIM
|
| pubmed:chemical | |
| pubmed:status |
MEDLINE
|
| pubmed:month |
Jan
|
| pubmed:issn |
0022-1767
|
| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:day |
1
|
| pubmed:volume |
138
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
157-63
|
| pubmed:dateRevised |
2003-11-14
|
| pubmed:meshHeading |
pubmed-meshheading:3537128-Animals,
pubmed-meshheading:3537128-Antibody Formation,
pubmed-meshheading:3537128-Antigen-Antibody Complex,
pubmed-meshheading:3537128-Autoantibodies,
pubmed-meshheading:3537128-Autoimmune Diseases,
pubmed-meshheading:3537128-B-Lymphocytes,
pubmed-meshheading:3537128-Cyclosporins,
pubmed-meshheading:3537128-Gene Expression Regulation,
pubmed-meshheading:3537128-Kidney Diseases,
pubmed-meshheading:3537128-Lymph Nodes,
pubmed-meshheading:3537128-Lymphatic Diseases,
pubmed-meshheading:3537128-Mice,
pubmed-meshheading:3537128-Mice, Inbred Strains,
pubmed-meshheading:3537128-Proto-Oncogene Proteins,
pubmed-meshheading:3537128-Spleen,
pubmed-meshheading:3537128-Synovitis,
pubmed-meshheading:3537128-T-Lymphocytes,
pubmed-meshheading:3537128-Thymus Gland
|
| pubmed:year |
1987
|
| pubmed:articleTitle |
CS-A therapy in MRL-lpr/lpr mice: amelioration of immunopathology despite autoantibody production.
|
| pubmed:publicationType |
Journal Article
|