| Project/Area Number |
60480150
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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 |
Experimental pathology
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| Research Institution | TOHOKU UNIVERSITY |
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Principal Investigator |
KYOGOKU Masahisa Tohoku University School of Medicine, 医学部, 教授 (70025542)
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| Co-Investigator(Kenkyū-buntansha) |
KATO Mitsuyasu Tohoku University School of Medichine, 医学部, 助手 (20194855)
SAWAI Takashi Tohoku University School of Medicine, 医学部, 助手 (00125577)
NOSE Masato Tohoku University School of Medicine, 医学部, 助教授 (70030913)
村上 一宏 東北大学, 医学部, 助手 (90190876)
宮沢 正顕 東北大学, 医学部付属病院, 助手 (60167757)
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| Project Period (FY) |
1985 – 1987
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| Project Status |
Completed (Fiscal Year 1987)
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| Budget Amount *help |
¥6,300,000 (Direct Cost: ¥6,300,000)
Fiscal Year 1987: ¥1,700,000 (Direct Cost: ¥1,700,000)
Fiscal Year 1986: ¥1,900,000 (Direct Cost: ¥1,900,000)
Fiscal Year 1985: ¥2,700,000 (Direct Cost: ¥2,700,000)
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| Keywords | granuloma / genetic analysis / polyarteritis / synovitis / rheumatoid arthritis / MRL / Mp-1pr / 1pr / 多発性動脈炎 / 遺伝的背景 / Class【II】抗原 / IL-1 |
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| Research Abstract |
In the socalled "Registered Intractable Diseases", We can find a number of chronic "Granulomatous" inflammations such as rheumatoid arthritis, polyarteritis, other collagen diseases, and even kawasaki disease. The etiopathogenesis of those diseases are still unknown. The purpose of this investgation is to find a clue to elucidate the etiopathogenesis of granulolma, which is mostly composed of macrophages, fibroblast, capillary and lymphocytes. Human cases such as rheumatoid synovitis, proliferated intima of various polyarteritis and animal models including MRL/MP-1pr/1pr mouse, BXSB and C3H/Hej-gld/gld has been the target of our examination.
1) Rheumatoid synovitis: Angiogenesis and proliferation of A cell type synovial cells are conspicuous at the beginning. CD4 T cell immigration and cuffing proliferation around high columnar endothelium are followed by secondary lymph follicle formation, which became the local center of IgG rheumatoid factor and self association immune complex. CD_4
… More
cells also made contact with synovial D cells and seemed to introduce a kind of delayed type hypersensitivity in joint. CD8 T cells are few in the site suggesting the ceaseless acceleration of immune network exist in the joint to destroy the hard tissues.
2) Polyarteritis: Proliferation of intima is remarkable in some type of polyarteritis making its prognosis very poor, most of which are granulomatous in nature. The main component of thickend intima is "activated myocyte", which proliferated in the media changing into secretory form after various growth factor stimulation, then immigrated to the intima where secrete various kinds of matrix one after another. GM1 ganglioside is a good marker of proliferation and the studies about the relation between genetic expression of cell marker,ie. development,and proliferation are going on at present.
3)MRL/Mp-1pr/1pr mouse: Arthritis, arteritis and glomerulitis of MRL/1 mouse are all granulomatous. macrophages stimulated and activated towards wrong direction by lpr dependent Thy 1.Ly 5+lymphocyte must be blamed as a major player in site to introduce marked tissue destruction. lpr gene (Yaa and gld genes either) seemed to be just a accerelator gene of such granulomatous lesion and socalled nephritogenic as well as vasculitogenic genes must be exist separately in the background gene complex. Less
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