| Project/Area Number |
10470086
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| Research Category |
Grant-in-Aid for Scientific Research (B).
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Immunology
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| Research Institution | EHIME UNIVERSITY |
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Principal Investigator |
ASANO Yoshihiro EHIME UNIVERSITY, SCHOOL OF MEDICINE, PROFESSOR, 医学部, 教授 (70114353)
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| Co-Investigator(Kenkyū-buntansha) |
SUMITA Kohsuke EHIME UNIVERSITY, SCHOOL OF MEDICINE, RESEARCH ASSOCIATE, 医学部, 助手 (20281454)
KANOH Makoto EHIME UNIVERSITY, SCHOOL OF MEDICINE, ASSISTANT PROFESSOR, 医学部, 講師 (10116923)
SHINOMIYA Hiroto EHIME UNIVERSITY, SCHOOL OF MEDICINE, ASSOCIATE PROFESSOR, 医学部, 助教授 (80162618)
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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 |
¥5,500,000 (Direct Cost: ¥5,500,000)
Fiscal Year 2000: ¥3,100,000 (Direct Cost: ¥3,100,000)
Fiscal Year 1999: ¥2,400,000 (Direct Cost: ¥2,400,000)
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| Keywords | IL-12 gene / cytokine / macrophage / dendritic cell / Listeria monocytogenes / 感染免疫 / T細胞サブセット / IL-12p40 / IRF-1 / マクロファージ機能 |
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| Research Abstract |
Pathogenic infections lead to activation of innate immunity followed by induction of a type 1 T cell subset, and therefore, provide a good model to evaluate when T cells commit to type 1 T cells. Here we show a two-step mechanism of T cell subsets commitment during pathogenic infection. The first step is mediated by the basal function of macrophage/dendritic cells and is antigen-independent. This step modulates the committed precursor frequency of T cell subsets and influences the expression of T-bet (T-box expressed in T cells ) and GATA-3 genes. The second step requires antigenic stimulation of T cells together with IL-12 or IL-4 and influences on the expression of T-bet and GATA-3. We propose a two-step T cell subset commitment pathway based on these observations. Therefore, pathogenic infections influence on functional T cell commitment before T cells encounter nominal antigen.
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