| Project/Area Number |
10672192
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Laboratory medicine
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| Research Institution | Kansai Medical University |
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Principal Investigator |
MASUDA Midori Kansai Medical University, Departments of Clinical Science and Laboratory Medicine, Associate Professor, 医学部, 講師 (50173753)
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| Project Period (FY) |
1998 – 1999
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| Project Status |
Completed (Fiscal Year 1999)
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| Budget Amount *help |
¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 1999: ¥1,100,000 (Direct Cost: ¥1,100,000)
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| Keywords | rheumatoid arthritis / autoimmune neutropenia / osteoarthrosis / atherosclerosis / FCγRIIIB / FcγRIIA / FcγRIIIA / polymorphism / genotype / 可溶性FcγR / リンパ球機能 |
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| Research Abstract |
Allelic variants of FcγR confer distinct phagocytic capacities providing a mechanism for heritable susceptibility to immune complex disease. Human FcγRIIa has two codominantly expressed alleles, R^<131> and H^<131>, which differ substantially in their ability to ligate human IgG2. Human FcγRIIIa has two alleles, F^<158> and F^<158>, which differ to ligate human IgG1 and IgG3. Human FcγRIIIb has two expressed alleles, NA1 and NA2, which differ to ligate human IgG3.
The distributions of allelic variants of FcγR in seeral desease were significantly different from those of healthy Japanese donors. The genotype of FcγRIIIB may affect desease activity of rheumatoid arthritis. The genotype of FcγRIIIB and FcγRIIA may affect the production of neutrophil specific auto-antibodies in autoimmune neutropenia of infancy and influence its clinical course. The genotype of FcγRIIIA may affect desease activity of osteoarthrosis. The genotype of FcγRIIIA and FcγRIIIB may affect desease activity of atherosclerosis.
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