1987 Fiscal Year Final Research Report Summary
Analysis of immune-regulatory cell functions in patients with chronic active hepatitis
Project/Area Number |
61570331
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Research Category |
Grant-in-Aid for General Scientific Research (C)
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Allocation Type | Single-year Grants |
Research Field |
Gastroenterology
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Research Institution | Tokyo Medical and Dental University |
Principal Investigator |
HASUMURA Yasushi School of Medicine, Tokyo Medical and Dental University, 医学部, 助教授 (40019956)
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Co-Investigator(Kenkyū-buntansha) |
IRIE Tetuya School of Medicine, Tokyo Medical and Dental University, 医学部, 助手 (70183192)
DAIGUJI Yuuichi School of Medicine, Tokyo Medical and Dental University, 医学部, 助手 (40155289)
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Project Period (FY) |
1986 – 1987
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Keywords | chronic active hepatitis / corticosteroid therapy / suppressor T cell activity / サプレッサーT細胞 |
Research Abstract |
Chronic active hepatitis(CAH) is characterized by periportal lymphocyte infiltration with hepatic cell necrosis(piecemeal necrosis) and the presence of circulating autoantibodies against the liver. Therefore, the disturbance in immune-regulatory system, in particular aginst the liver, has been thought to play a role in the pathogenesis, but its nature remains unknown. To clarify this, the function of T lymphocytes in the peripheral blood was tested in 12 patients with CAH both before and after the corticosteriod theraphy for 8 weeks. By the therapy, six patients had a clear improvements in the clinical symptoms and laboratory data, thus it was defined these six as a corticosteroid theraphy-effective group. Other six patients showed no particular improvements, and were classified as an ineffective group. Before the corticosteroid therapy, the activity of suppressor T cell was found to be significantily lower in both the corticosteroid therapy-effective and ineffective groups than in heal
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thy controls. Concomitantly, the responce in T lymphocytes to interleukin-2(IL-2) was low in the two CAH groups as compared with controls. It is noteworthy, however, that the reduced T lymphocyte functions returned to the normal range when the patients were treated with the corticosteroid administration and had the clinical improvement. By contast, in the ineffective group, no recovery of the T lymphocyte functions was observed even after the corticosteroid therapy. The improvement in the T lymphocyte functions was also observed only in the corticosteroil-effective group when the activity or responce was tested in the pretreated T lymphocytes in the presence of prednisolone. Thus, it is conceivable that in CAH, T lymphocyte function reflects to the activity of the disease. The production of IL-2 by the circutating T lumphocytes was also tested and found to be normal in both CAH groups. However, the production rate of prostaglandin E in the circulating macrophages was low in the patients. These results suggest that the disturbance in the T lymphocyte function plays a significant role in the pathogenesis of CAH thus the corticosteroid effect in CAH is due, at least in part, to an immunomodulation in T luymphocyte function. Less
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