| Project/Area Number |
10670510
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Gastroenterology
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| Research Institution | JIKEI UNIVERSITY SCHOOL OF MEDCINE |
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Principal Investigator |
TAKAHASHI Hiroki JIKEI UNIVERSITY SCHOOL OF MEDICINE, DIVIGION OF GASTROENTEROLOGY AND HEPATOLOGY, DEPARTMENT OF INTERNAL MEDICINE, ASSISTANT, 医学部, 助手 (80256403)
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| Co-Investigator(Kenkyū-buntansha) |
ZENIYA Mikio JIKEI UNIVERSITY SCHOOL OF MEDICINE, DIVIGION OF GASTROENTEROLOGY AND HEPATOLOGY, DEPARTMENT OF INTERNAL MEDICINE, ASSISTANT PROFESSOR, 医学部, 助教授 (70138767)
TODA Gotaro JIKEI UNIVERSITY SCHOOL OF MEDICINE, DIVIGION OF GASTROENTEROLOGY AND HEPATOLOGY, DEPARTMENT OF INTERNAL MEDICINE, PROFESSOR, 医学部, 教授 (40090500)
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| Project Period (FY) |
1998 – 2000
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| Project Status |
Completed (Fiscal Year 2000)
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| Budget Amount *help |
¥3,100,000 (Direct Cost: ¥3,100,000)
Fiscal Year 2000: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 1999: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 1998: ¥1,200,000 (Direct Cost: ¥1,200,000)
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| Keywords | AUTOIMMUNE HEPATITIS / NKT / TOLERANCE / Vα24 / CD1d / CD1b / CDLd / Vα24JαQ |
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| Research Abstract |
Background : Defect of self-tolerance is one of the main pathogenesis of autoimmune disease. Since NKT cell has been reported to decrease at the onset of autoimmune disease, it may participate in the maintenance of self-tolerance. The aim of this study is to clarify the role of NKT cell in the pathogenesis of autoimmune liver disease.
Methods : Clinically and histologically diagnosed 6 autoimmune hepatitis (AIH), 8 primary biliary cirrhosis (PBC) and 20 type C chronic hepatitis (CHC) patients were studied. Detection of NKT cell specific Vα24 JαQ gene fragment in the liver was performed by two step PCR using Vα24 sense/Cα antisense primer and Vα24 sense/JαQ antisense primer.
Results : Vα24 JαQ gene fragment was detected in 50% of AIH, 100% of PBC and CHC.Histological activity and ALT level of NKT negative AIH patients were much severe compared with positive patients. Prednisolon therapy was required for NKT negative AIH patients, but UDCA therapy was enough for NKT positive AIH patients.
Conclusion : Selective reduction of NKT cells was observed in AIH patients with severe activity. The results suggest that NKT cell participates in the pathogenesis of AIH.
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