| Project/Area Number |
16590630
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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 | Keio University |
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Principal Investigator |
OKAMOTO Susumu Keio University, Department of Medicine, Instructor, 医学部, 助手 (70255446)
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| Co-Investigator(Kenkyū-buntansha) |
HIBI Toshifumi Keio University, Department of Medicine, Professor, 医学部, 教授 (50129623)
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| Project Period (FY) |
2004 – 2005
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| Project Status |
Completed (Fiscal Year 2005)
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| Budget Amount *help |
¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 2005: ¥1,600,000 (Direct Cost: ¥1,600,000)
Fiscal Year 2004: ¥2,000,000 (Direct Cost: ¥2,000,000)
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| Keywords | IBD / T cell / Th1 / SAP |
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| Research Abstract |
We examined SAP expression in CD4 T cells from IBD murine models as well as IBD patients. Though in animal models SAP expression tended to be lower in CD4 T cells from inflamed colonic tissue compared to normal tissue both at transcription and protein level. However, in samples from IBD patients, we could not observe any difference among normal controls, UC and CD patients. As it has been reported that SAP deficient T cells have profound defect in differentiation into Th2 cells in contrast to SAP transgenic T cells, which are biased towards Th2 differentiation, we next performed in vivo animal studies to clarify the role of SAP in chronic intestinal inflammation. For CD4 transfer colitis model, we purified CD45RBhi CD4 T cells from wild-type, SAP knockout, and SAP transjenic mice as donor cells. However, we could not observe any significant difference in severity of colitis among the three groups. We think that these negative data paradoxically highlight the complicated mechanism of mucosal immune regulation.
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