| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2013: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2012: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
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| Research Abstract |
The transcription factor Bcl11b plays key roles in T cell development and T cell-mediated immune responses. We examined thymocytes at and after the DP stage in a series of Bcl11b-attenuated mutant mice that carry conditional-knockout and ENU-induced hypomorphic alleles. We show that Bcl11b impairment leads to an increased production of TCRbeta highCD44highCD122high innate CD8+SP thymocytes, which express Eomes and secrete IFN-gamma rapidly after the stimulation with PMA and ionomycin. Since NKT cells in these Bcl11b-mutant mice exhibit developmental arrest at multiple steps, increase of innate CD8SP is not likely to be caused by bystander NKT cells. These results indicate that Bcl11b regulates development of different thymocyte subsets at multiple stages and prevents excessive innate CD8+SP thymocyte differentiation.
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