The analysis of novel mechanisms of lineage commitment to CD4+/CD8+ thymocytes based on identification of a kinase that is critical for CD4+T cell development

Research Project

Project/Area Number	25860365
Research Category	Grant-in-Aid for Young Scientists (B)
Allocation Type	Multi-year Fund
Research Field	Immunology
Research Institution	Kyushu University
Principal Investigator	ISHIKAWA ERI 九州大学, 生体防御医学研究所, 助教 (20546478)
Project Period (FY)	2013-04-01 – 2015-03-31
Project Status	Completed (Fiscal Year 2014)
Budget Amount *help	¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000) Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000) Fiscal Year 2013: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
Keywords	T細胞分化 / シグナル伝達 / セリンスレオニンキナーゼ
Outline of Final Research Achievements	We have found that PKD is phosphorylated upon stimulation with peptides in preselection DP thymocytes. We then established T cell-specific PKD deficient mice and found that CD4+ single positive thymocytes were specifically decreased in the mice. From the finding, we aimed to elucidate the molecular mechanisms of lineage commitment into CD4+/CD8+ thymocytes by the analysis of the mice. In PKD-deficient mice, TCR signal was attenuated and CD4+ T cell development was more affected than CD8+ T cell. We identified some TCR stimulation-dependent substrates of PKD by proteomic analysis. Phosphorylation of one of these substrates has been revealed to contribute to thymocyte development.

Report

(3 results)