| Project/Area Number |
03670212
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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 |
細菌学
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| Research Institution | Osaka University |
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Principal Investigator |
KINOSHITA Taroh Osaka University Research Institute for Microbial Diseases, 微生物病研究所, 教授 (10153165)
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| Project Period (FY) |
1991 – 1992
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| Project Status |
Completed (Fiscal Year 1992)
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| Budget Amount *help |
¥1,900,000 (Direct Cost: ¥1,900,000)
Fiscal Year 1992: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 1991: ¥1,300,000 (Direct Cost: ¥1,300,000)
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| Keywords | Self defense / Complement / Complement receptor / 補体レセプタ- |
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| Research Abstract |
Complement is activated on the surface of microorganisms antibody-dependently and -independently. C3b molecules are deposited on the microbial surfaces as clusters. The C3b molecules are subsequently degraded to iC3b and then to C3dg. These C3 fragments act as ligands of complement receptors expressed on various cells that participate in self defense system. This study aimed to elncidate roles of complement and complement receptors in the self defense system. We made following findings.
1. Within the classical pathway C5 convertase C3b binds to specific Ser residue of C4b (Ser 1217 in the human and Ser 1213 in the mouse).
2. We evaluated roles of complement receptors CR1 and CR2 in the humoral immune response by injecting mice with monoclonal antibody (7G6) that is capable of down-modulating mouse CR1 and CR2 on B-lymphocytes and of inhibiting C3d-binding to these receptors. Animals treated with 7G6 responded very weakly to the limited doses of thymus-dependent and -independent antigens. These results elarified important roles of complement receptors in antibody response.
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