| Project/Area Number |
05807065
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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 |
Pediatrics
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| Research Institution | Kochi medical school |
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Principal Investigator |
TOMODA Takashi Kochi Medical school, Pediatrics, Associate, 医学部, 助手 (20207632)
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| Co-Investigator(Kenkyū-buntansha) |
KURASHIGE Takanobu Kochi Medical school, Pediatrics, Professor, 医学部, 教授 (50117032)
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| Project Period (FY) |
1993 – 1994
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| Project Status |
Completed (Fiscal Year 1994)
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| Budget Amount *help |
¥1,900,000 (Direct Cost: ¥1,900,000)
Fiscal Year 1994: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1993: ¥1,400,000 (Direct Cost: ¥1,400,000)
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| Keywords | IDDM / IL-2 / HLA-DR / beta-cell / IL-2 system / IL-4 / T heper land 2 |
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| Research Abstract |
The pathogenesis of imsulin-dependent disbetes mellitus(IDDM) remains obscure, however, since the discovery of islet cell antibody, immunological abnormalities are now believed to contribute to the pathogenesis of IDDM.In this study, the production on interleukin 2 (IL-2), the responses to IL-2 and IL-2 receptor expression by peripheral blood T lymphocytes were compared in IDDM and normal non-diabetic children. In IDDM,IL-2 production by CD4-positive T cells within the IL-2 system is thought to be selectively defective.
However, it is obscure that defective productin of IL-2 is either cause or result of IDDM.The target antrigen of CD4 positrve T cells is HLA-DR on beta-cell. In IDDM,HLA-DR antigens expressed on beta-cell, were markedly enhanced in compare with non diabetics.
Thus, we are studing this mechanisms using more mouse tumor cell line of pancreas beta-cell.
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