Role of anti-DNA antibody and anti-cardiolipin antibody for the progression of vasculopathy in collagen diseases
| Project/Area Number |
01570348
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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 | Chiba University |
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Principal Investigator |
KOIKE Takao Chiba University School of Medicine, Assistant, 医学部・第二内科, 助手 (80146795)
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| Project Period (FY) |
1989 – 1990
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| Project Status |
Completed (Fiscal Year 1990)
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| Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1990: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 1989: ¥1,200,000 (Direct Cost: ¥1,200,000)
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| Keywords | systemic lupus erythematosus / anti-phospholipid antibody / anti-cardiolipin antibody / anti-DNA antibody / lupus nephritis / thrombosis / fetal loss / V region gene / 血管病変 / 流・早産 / ハイブリド-マ |
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| Research Abstract |
To clarify the specificity of anticardiolipin antibody (aCL), we developed 18 monoclonal hybridoma aCL from SLE prone, MRL-1pr/1pr mice and the reactivity of these antibodies to phospholipids, DNA, epithelial cells (HEp-2 cells), platelets, endothelial cells, heparin, protein C and thrombomodulin was examined. All the monoclonal aCL reacted with phosphatidylserine and 11 of 18 also reacted with phosphatidylinositol. Three of 18 hybridoma aCL bound to both ssDNA and dsDNA, and 10 of 18 bound to ssDNA but not to dsDNA. The characteristics of antinuclear antibody were manifest for 10 of 18 monoconal aCL reacted with platelets. Three of 18 monoclonal aCL bound to vascular endothelial cells and these monoclonal aCL also had a strong reactivity to heparin. No monoclonal aCL showed reactivity to protein C or to thrombomodulin.
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Report
(3 results)
Research Products
(32 results)
