| Project/Area Number |
02670289
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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 Tokai University, Dept.of Medicine, Professor of Medicine, 医学部・内科, 教授 (80102846)
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| Co-Investigator(Kenkyū-buntansha) |
YAGAME Mitsunori Tokai Univ.Dept.of Medicine Instructor of Medicine, 医学部・内科, 助手 (10210212)
MIURA Masahiko Tokai University, Dept.of Medicine, Assistant Professor of Medicine, 医学部・内科, 講師 (00190596)
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| Project Period (FY) |
1990 – 1992
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| Project Status |
Completed (Fiscal Year 1992)
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| Budget Amount *help |
¥2,500,000 (Direct Cost: ¥2,500,000)
Fiscal Year 1992: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 1991: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 1990: ¥700,000 (Direct Cost: ¥700,000)
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| Keywords | IgA nephropathy / Hyperproduction of IgA / Switch T cell / IL-4 / IL-5 / TGF-beta / IL-6 / IgA産生能 / サイトカイン / ILー4 / ILー5 / ILー6 / TGFーβ / T_<α4>細胞 |
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| Research Abstract |
It is well known that IgA nephropathy is mediated by IgA-dominant immune complexes although the pathogenesis for inducing such immune complexes is unknown.
The aim of the present study was to elucidate cytokines which are responsible for increased production of IgA observed in patients with IgA nephropathy and in some of their relatives. Fifty six patients with IgA nephropathy and 96 family members were studies. Fifty four healthy adults were served as controls. Peripheral blood mononuclear cells (PBMC) were separated and B-cell rich fraction as well as Talpha4 cells (i.e.IgA specific helper T cells) were concentrted by immune absorption technique. Interleukin 4, 5 aad 6 (IL-4, IL-5, IL-6) and tissue growth factor (TGF-beta) were cocultured with these B and T cell cultures alone or in combined forms. IgG, IgA, and IgM-bearing cells in these cultures were quantitated by flow cytometry. Concentration of IgG, IgA, IgM and IgE were measured by ELISA.
There was no significant increase of IgA production in cultures with IL-5, IL-6 and TGF-beta. However, IL-4 induced significant increase in IgA-bearing cells and supernatant IgA in cultures with this cytokine with and without addition of IL-6.
IL-6 did not induce IgA-specific helper activity when added to lymphocyte cultures alone but significantly enhanced IgA production when added with IL-4. It is concluded that IL-4 is the cytokine which specifically induce IgA in humans while IL-5 and TGF-beta show such activity in mice. Further sutdies are warranted to explore clinical significance of IL-4 and IL-6 in patients with IgA nephropathy.
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