| Project/Area Number |
62570300
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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 |
内科学一般
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| Research Institution | Tokai University |
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Principal Investigator |
SAKAI Hideto School of Medicine, Tokai University, Department of Internal Medicine, Professor, 医学部・内科, 教授 (80102846)
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| Co-Investigator(Kenkyū-buntansha) |
SUGA Takao School of Medicine, Tokai University, Department of Internal Medicine, Instructo, 医学部・内科, 助手 (50187621)
ENDO Masayuki School of Medicine, Tokai University, Department of Internal Medicine, Assistant, 医学部・内科, 講師 (10147134)
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| Project Period (FY) |
1987 – 1989
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| Project Status |
Completed (Fiscal Year 1989)
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| Budget Amount *help |
¥2,800,000 (Direct Cost: ¥2,800,000)
Fiscal Year 1989: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 1988: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 1987: ¥900,000 (Direct Cost: ¥900,000)
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| Keywords | IgA nephropathy / Switch T cells / CD4 / IgA / IgA産生能亢進 / 家族性免疫異常 / T_<α4>細胞 / IgA産生 / IgA産生亢進 / ヘルパーT細胞 |
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| Research Abstract |
Enumeration and functional analysis of CD4^+ T cells with receptors for the Fc portion of IgA (i.e. Talpha4 cells) in the peripheral blood or patients with IgA nephropathy, their relatives and age-matched controls were performed to elucidate polyclonal activation of IgA production in this disease. Enumeration of Talpha4 cells was performed by a fluorescence activated cell sorter, and functional analysis was carried out by separation of Talpha4 cells, and IgM-, IgA- and IgG-bearing lymphocytes using panning methods followed by cultures of these cells for 7 days with pokewecd mitogen. There was a significant increase in the amount of peripheral blood Talpha4 cells in patients with IgA nephropathy and their relatives. Talpha4 cells specifically enhanced the switch of IgM-bearing cells to IgA-bearing cells, and this switch activity was inhibited by addition or human myeloma IgA. It is suggested that Talpha4 cells may be responsible for polyclonal activation of IgA production in IgA nephropathy.
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