| Project/Area Number |
62570222
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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 |
Immunology
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| Research Institution | University of Occupational and Environmental Health |
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Principal Investigator |
YAMASHITA Uki Associate Professor, Department of Immunology, University of Occupational and Environmental Health, Sch Med., 医学部・免疫学教室, 助教授 (00028680)
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| Project Period (FY) |
1987 – 1988
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| Project Status |
Completed (Fiscal Year 1988)
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| Budget Amount *help |
¥2,400,000 (Direct Cost: ¥2,400,000)
Fiscal Year 1988: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 1987: ¥1,600,000 (Direct Cost: ¥1,600,000)
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| Keywords | Interleukin 1 / Interleukin 1 receptors / T lymphocytes / B lymphocytes / Macrophages / HLA-DR antigens / 細胞間相互作用 / 単球 / HLA-DR抗原 |
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| Research Abstract |
Interleukin 1 (IL 1) produced by macrophages plays an important role for the regulation of many kinds of immune responses. In this paper the author studied the role of macrophages and IL 1 in the induction of immune responses using human systems and obtained the following results.
1: Purified T cells and B cells alone were not activated by the stimulation with antigens or mitogens. However, the addition of HLA-DR-positive macrophages successfully activated T cells and B cells to proliferate, to produce lymphokines and to differentiate into antibody forming cells. A part of these macrophage functions could be replaced with IL 1.
2: The action of il 1 to the cells is performed through receptors (IL 1R) on the cells.
3: IL 1R are specific for IL 1. The binding of labeled IL 1 to IL 1R was inhibited by unlabeled IL 1, but not by other lymphokines. IL 1 and IL 1 share the same IL 1R.
4: IL 1R were not expressed on resting lymphccytes. However, they were promptly induced on the lymphocytes after the stimulation with antigens. The expression of IL 1R on T cells requires the accessory functions of HLA-DR-positive macrophages. The depletion of macrophages from the T cell population and the addition of anti-HLA-DR antibody inhibited the expression of IL 1R on T cells. The expression of IL 1R on B cells was also inhibited by the addition of anti-HIA-DR antibody. These results suggest that the expression of IL 1R on T cells and B cells is induced by the results of T cell-macrophage inter-actions and B cell-B cell interactions mediated by antigens and HLA-DR antigens and the binding of IL 1 on IL 1R induces the activation of T cells and B cells.
5: after the binding of IL 1 to the cells, the level of intracellular cyclic AMP was increased and the signal of IL 1 was transduced into the cells.
6: Adult T cell leukemia cells and B cells from patients with systemic lupus erythematosus produced IL 1 and expressed IL 1R and IL 1 functioned an autocrine growth factor for these cells.
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