Role of anti-endothelial cell antibodies and transendothelial migratory T cells in the pathogenesis of autoimmune lesions
| Project/Area Number |
06670495
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
内科学一般
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| Research Institution | Jichi medical School |
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Principal Investigator |
KANO Shogo Faculty of Medicine, Jichi medical School Prof., 医学部, 教授 (00049024)
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| Project Period (FY) |
1994 – 1995
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| Project Status |
Completed (Fiscal Year 1995)
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| Budget Amount *help |
¥2,400,000 (Direct Cost: ¥2,400,000)
Fiscal Year 1995: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 1994: ¥1,400,000 (Direct Cost: ¥1,400,000)
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| Keywords | Rheumatoid arthritis / Systemic lupus erythematosus / Ribosomal P0 protein / Transendothelial migration / Anti-endothelial cell antibody / Autoimmunity / T cells |
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| Research Abstract |
Anti-endothelial cell antibody levels are elevated in sera from systemic lupus erythematosus (SLE) patients, especially in those who had pulmonary hypertension, digital vasculitis, Raynaud's phenomenon, or serositis. The antigens reacting with anti-endothelial cell antibodies is shown to be 36,37kD proteins by immunoblotting. The analysis of the cloned cDNA from human placenta cDNA library confirmed ribosomal P0 protein as the antigen. Enzyme-linked immunosorbent assay for anti-ribosomal P0 protein antibodies was established using recombinant fusion protein derived from cDNA as antigens. Anti-ribosomal P0 antibodies were positive only in sera from SLE patients, and positive anti-ribosomal P0 protein antibodies were correlated with central nervous system involvement other than lupus psychosis.
Rheumatoid arthritis is characterized by chronic inflammation of synovium resulting in destruction of bone and cartilage of joints. Trans-endothelial migration of T cell subsets with surface phenotype of LFA-1 (intermediately positive), CD26 (highly positive) is involved in the pathogenesis of chronic synovitis. In vitro antigen-stimulated activation of those T cell subset is suppressed by disease-modifying anti-rheumatic drugs such as gold sodium thiomalate, auranofin or bucillamine. The greater level of suppression was observed in patients whoresponded the medication, indicating possible predicting value for these assessment
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Report
(3 results)
Research Products
(12 results)
