Molecular mechanisum of memory CD8 T cell differentiation

2014 Fiscal Year Final Research Report

• Project/Area Number: 24590573
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Immunology
• Research Institution: Chiba University
• Principal Investigator: SAKAMOTO Akemi 千葉大学, 医学(系)研究科(研究院), 助教 (90359597)
• Co-Investigator(Kenkyū-buntansha): TOKUHISA Takeshi 千葉大学, 学長 (20134364)
• Project Period (FY): 2012-04-01 – 2015-03-31
• Keywords: メモリーＴ細胞 / ＣＤ８Ｔ細胞 / Ｂｃｌ６ / 転写因子 / サイトカイン

Outline of Final Research Achievements

Bcl6, a sequence specific transcriptional repressor, is important for generation and maintenance of central memory CD8+ T cells. However, the molecular mechanism involved in the generation is largely unknown. We demonstrated that Bcl6 negatively regulates the in vivo differentiation of both activated CD25+ CD8+ T cells and KLRG1hi effector CD8+ T cells. Since the induction of CD25 expression was more rapid and the amount of phosphorylated STAT5 was higher in the in vitro activated Bcl6-deficient CD8+ T cells than in the activated wild type CD8+ T cells, the IL-2 signaling was negatively regulated in activated CD8+ T cells by Bcl6. We also confirmed the Bcl6 binding to the various regions in the CD25 and IL-2 genes. These results indicate that Bcl6 is responsible for the differentiation of memory precursor CD8+ T cells by regulating the IL-2 signaling in activated CD8+ T cells.

Free Research Field

免疫学