| Project/Area Number |
02454255
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Circulatory organs internal medicine
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| Research Institution | Kyoto University |
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Principal Investigator |
MATSUMORI Akira Kyoto University Dep. of Internal Med. Assistant Professor, 医学部, 講師 (70135573)
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| Project Period (FY) |
1990 – 1991
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| Project Status |
Completed (Fiscal Year 1991)
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| Budget Amount *help |
¥5,300,000 (Direct Cost: ¥5,300,000)
Fiscal Year 1991: ¥2,000,000 (Direct Cost: ¥2,000,000)
Fiscal Year 1990: ¥3,300,000 (Direct Cost: ¥3,300,000)
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| Keywords | Cardiomyopathy / Myocarditis / Virus / Autoantibody / Anti-heart antibody / Auto-immunity / Monoclonal antibody / Hybridoma / 心筋炎 / ハイブリド-マ |
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| Research Abstract |
In order to clarify the role of antiheart antibody in the pathogenesis of myocarditis and cardiomyopathy, we analyzed anti-heart antibody by developing monocional antibodies. Anti-heart autoantibodies were found in the sera from Balb/c mice with myocarditis infected with encephalomyocarditis (EMC) virus. Frozen sections of the hearts of uninfected mice were incubated with mouse sera and stained with anti-mouse lgG and lgM. Positive granular staining was first seen on day 4 and persisted to day 90 ; the titer was highest on day 21. Spleen cells from mice with positive anti-heart antibody on day 21 at post-infection were fused with a cell line of plasmacytoma. Supernatants of hybridoma were screened by immunoflurerescence against murine heart sections. Two clones of lgM-producing hybridoma were developed ; one clone IA5, stained myocytes with striated pattern and the other clone IB5, stained endothelial cells. Results from western immunoblotting analyses demonstrated that IA5 reacted with cardiac myosin. These studies suggest that myosin is one of the major autoantigens in EMC virus myocarditis.
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