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

2014 Fiscal Year Final Research Report

• 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
• 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.

Free Research Field

免疫学