| Project/Area Number |
63480193
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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 |
内科学一般
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| Research Institution | Saitama Medical Center, Saitama Medical School |
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Principal Investigator |
ABE Tohru Saitama Medical Center 2nd Department of Medicine Professor, 総合医療センター 第2内科, 教授 (60051207)
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| Co-Investigator(Kenkyū-buntansha) |
HOSONO Osamu Saitama Medical Center 2nd Dep. Int. Med., 総合医療センター 第2内科, 助手 (50190210)
TAKEUCHI Tsutomu Saitama Medical Center 2nd Dep. Int. Med. Assistant Professor, 総合医療センター 第2内科, 講師 (50179610)
TAKANO Makoto Saitama Medical Center 2nd Dep. Int. Med. Associate Professor, 総合医療センター 第2内科, 助教授 (90101021)
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| Project Period (FY) |
1988 – 1989
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| Project Status |
Completed (Fiscal Year 1989)
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| Budget Amount *help |
¥4,800,000 (Direct Cost: ¥4,800,000)
Fiscal Year 1989: ¥2,000,000 (Direct Cost: ¥2,000,000)
Fiscal Year 1988: ¥2,800,000 (Direct Cost: ¥2,800,000)
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| Keywords | rheumatoid arthritis / rheumatoid factor / bacterial infection / anti-idiotypic antibody / Fc結合蛋白 / 関節症状 / プロテインA / 微生物 |
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| Research Abstract |
Rheumatoid arthritis (RA) is a systemic multi-organic inflammatory disease or unknown etiology, affecting joints and manifesting with striking immune abnormalities. Because of the immune abnormalities, RA is associated with the formation of auto-antibodies such as rheumatoid factor and anti-nuclear antibodies. In the form of immune complexes, these auto-antibodies, especially rheumatoid factor, are implicated in the pathogenesis of joint destruction.
We described the presence of anti-idiotypic antibody in a patient with monoclonal IgM with rheumatoid factor activity 2weeks after pneumococcal bacteremia, which resulted in 1% marked reduction of rheumatoid factor activity. Next we raised monoclonal anti-idiotypic antibody against Ka m-RF and searched for cross-idiotypic determinants on polyclonal IGM-RF from unrelated individuals with rheumatoid arthritis. By, using lymphocytes from RA patients with cross-idiotypic antigen, we investigated the effect of the anti-idiotypic antibody on in vitro RF production.
Pretreatment of patients' peripheral blood lymphocytes by the relevant anti-idiotypic antibody (hybridoma ascites IgG) resulted in a marlied reduction of rheumatoid factor production by lymphocytes from patients who appear to have shared idiotypes with our patient's monoclonal idiotypes.
Furthermore, 30% of patients with RA had anti-protein A antibody. These results support the hypothesis that rheumatoid factor arise as an anti-idiotypic antibodies against anti protein A antibody.
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