| Project/Area Number |
09670577
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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 | The JIKEI University School of Medicine |
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Principal Investigator |
AIZAWA Yoshio The JIKIE University School of Medicine, Faculty of Medicine, Lecturer, 医学部, 講師 (90147273)
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| Co-Investigator(Kenkyū-buntansha) |
FUKADA Hiroyuki The JIKIE University School of Medicine, Faculty of Medicine, Fellow, 医学部, 助手 (60287282)
TAKAHASHI Hiroki The JIKIE University School of Medicine, Faculty of Medicine, Fellow, 医学部, 助手 (80256403)
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| Project Period (FY) |
1997 – 1999
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| Project Status |
Completed (Fiscal Year 1999)
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| Budget Amount *help |
¥2,600,000 (Direct Cost: ¥2,600,000)
Fiscal Year 1999: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 1998: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 1997: ¥1,300,000 (Direct Cost: ¥1,300,000)
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| Keywords | Autoimmune Hepatitis / asialoglycoprotein receptor / Cre-loxP transgenic mouse / animal model / 再燃 / ステロイド / Th1サイトカイン / Th2サイトカイン / CD80 / 肝特異抗原 / 抗アシアログリコプロテインレセプター抗体 / 遺伝子導入 |
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| Research Abstract |
To clarify the molecular immuno-mechanisms of the autoimmune liver disease, we plan to establish the animal model which express asialoglycoprotein receptor (ASGPR) permanently or transiently on the surface of the hepatocyte and to clarify the importance of anti ASGPR antibody (anti-ASGPR) on the autoimmune hepatitis (AIH) by using trasgenic technics especialy by newly developed Cre-nox transient gene expression technic. As shown in our study, the level of anti-asialoglycoprotein recetor antibody (anti-ASGPR) in the active phase of AIH was very high and it seemed to participate in the pathogenesis of active phase of AIH. However, another chronic liver disease such as chronic hepatitis Corprimaly biliary cirrhosis, it was not increasing. Interestingly, anti-ASGPR became lower after prednisone therapy.
We try to establish animal model in which human ASGPR was continuosly or transiently expressed on the surface of the hepatocytes using transgenic technology with alubmin promotor. However, we can not make a good animal model for autoimmune hepatits.
For further study, we should establish animal model for autoimmune liver disease, by which the molecular immnuno-mechanisms of autoimmune liver disease can be more clearly clarified.
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