| Project/Area Number |
09670146
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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 |
Pathological medical chemistry
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| Research Institution | University of Tsukuba |
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Principal Investigator |
TAKAHASHI Satoru University of Tsukuba, Institute of Basic Medical Sciences, Lecturer., 基礎医学系, 講師 (50271896)
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| Co-Investigator(Kenkyū-buntansha) |
YAMAMOTO Masayuki University of Tsukuba, Institute of Basic Medical Sciences, Professor, 基礎医学系, 教授 (50166823)
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| Project Period (FY) |
1997 – 1998
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| Project Status |
Completed (Fiscal Year 1998)
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| Budget Amount *help |
¥2,900,000 (Direct Cost: ¥2,900,000)
Fiscal Year 1998: ¥1,300,000 (Direct Cost: ¥1,300,000)
Fiscal Year 1997: ¥1,600,000 (Direct Cost: ¥1,600,000)
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| Keywords | c-Maf / GATA-3 / Transgenic mouse / T lymphocyte / Autoimmune disease / Transcription factor |
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| Research Abstract |
The susceptibility to various diseases including autoimmune diseases is closely related to the balance between T lymphocyte subpopulations (Th1 cells vs. Th2 cells). According to the recent reports, Th2 cells were induced by c-Maf or/and GATA-3 which activates the transcription of IL-4 gene. On the basis of these results, we intended to regulate disease susceptibility by utilizing c-Maf for changing the balance between Th1 and Th2 cells.
(1) Generation of transgenic mice which express c-Maf in T lymphocyte lineage.
Transgenic mice were generated which express c-Maf or/and GATA-3 under the gene regulatory system of CD2 or LCK in T lymphocytes. Th2 cells were dominant in the mice from the serological analysis. The mice also frequently suffered from lymphoma after 8-10 months old. We are planning to introduce the transgene to the background which develop autoimmune diseases spontaneously and to see whether these transgenes will change the disease severity.
(2) Gene disruption of mouse c-maf gene.
We generated null mutant of c-maf gene. c-Maf null mice were mostly lethal at the late stage of embryogenesis and showed defective lens formation. We will search for the influence on T lymphocyte differentiation in the mutant mice.
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