1994 Fiscal Year Final Research Report Summary
Analysis of the mechanism of abnormal T cell function in Behcet's disease
| Project/Area Number |
05670433
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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 | Teikyo University |
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Principal Investigator |
HASHIMOTO Takashi Teikyo University, School of Medicine, Associate Professor, 医学部, 助教授 (30082142)
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| Co-Investigator(Kenkyū-buntansha) |
YAMAGIDA Tamiko Teikyo University, School of Medicine, Assistant, 医学部, 助手 (80082204)
HARAOKA Hitomi Teikyo University, School of Medicine, Assistant, 医学部, 助手 (60228632)
HIROHATA Shunsei Teikyo University, School of Medicine, Lecturer, 医学部, 講師 (90189895)
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| Project Period (FY) |
1993 – 1994
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| Keywords | Behcet's disease / Rheumatoid arthritis / T lymphocyte / IFN-gamma / Superantigens / Monocyte / Anti-CD3 / T cell receptor |
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| Research Abstract |
There have been several lines of evidence suggesting the involvement of abnormal T lymphocytes activation in the pathogenesis of Behcet's disease. The current studies were undertaken to delineate the mechanism of abnormal T cell responses in Behcet's diesase. T cells from patients with Behcet's disease as well as those from normal individuals were stimulated with high concentrations of Staphylococcal enterotoxin (SE) A or C1 (0.1 ng-0.1 mug/ml) to produce comparable amounts of IFN-gamma. By contrast, T cells from patients with Behcet's disease produced significantly higher amounts of IFN-gamma than those from normal individuals or from patients with rheumatoid arthritis (RA) upon stimulation with low concentrations of SEA or SEC1(1 pg/ml). In addition, T cells from patients with Behcet's disease as well as those from RA patients were stimulated with either high or low concentrations of immobilized anti-CD3 to produce comparable amounts of IFN-gamma. Monocytes from RA patients supported the abnormal responses of T cells from Behcet's disease patients to SEC1. However, monocytes from Behcet's disease patients did not result in the abnormal reponses of T cells from RA patients to SEC1. These results suggest that T cell hypersensitivity in Behcet's disease might be a result of an abnormal signal transduction between T cell receptor Vbeta chains and CD3 molecules.
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