| Project/Area Number |
12670481
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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 | KYOTO UNIVERSITY |
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Principal Investigator |
WAKTSUKI Yoshio Graduate School of Medicine, Kyoto University Lecturer, 医学研究科, 講師 (40220826)
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| Project Period (FY) |
2000 – 2001
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| Project Status |
Completed (Fiscal Year 2001)
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| Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2001: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 2000: ¥2,900,000 (Direct Cost: ¥2,900,000)
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| Keywords | experimental colitis / animal model / immunology / gastroenterology / Biotechnology / ulcerative colitis / Crohns' disease / pathogenesis |
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| Research Abstract |
Immunological pathogenesis of inflammatory bowel diseases such as ulcerative colitis and Crohn's disease is not fully understood. Recent reports based on clinical studies as well as studies on experimental colitis models indicate that an abrogation of immune tolerance to luminal microbial antigens by the host plays an important role in the pathogenesis.
In order to elucidate the mechanism how break down of immunological tolerance in the intestine leads to onset and maintenance of the disease, the animal models which allow us to investigate antigen specific imunoregulation in the affected organ are imperative. We have established a novel colitis model utilizing adoptive transfer of CD4 T cells bearing OVA-specific TcR to mice inoculated with E.coli producing OVA. We also employed OVA-TcR Tg mice crossed to mice with disruption in Rag2 gene or genes of lymphokines as donor mice for cell transfer studies. We have established colitis in the recipient mice with histological features very similar to human ulcerative colitis. We have described histological features of the disease and analyzed cellular mechanism leading to colitis in this model by identifying colitogenic as well as regulatory CD4 T cells.
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