Notch signal controls the survival of memory CD4+ T cells

2014 Fiscal Year Final Research Report

• Project/Area Number: 24590585
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Immunology
• Research Institution: Gifu University
• Principal Investigator: MAEKAWA Yoichi 岐阜大学, 医学(系)研究科(研究院), 教授 (10294670)
• Project Period (FY): 2012-04-01 – 2015-03-31
• Keywords: 免疫記憶 / メモリーCD4陽性T細胞 / Notchシグナル / グルコース代謝 / Akt

Outline of Final Research Achievements

CD4+ T cells differentiate into memory T cells that protect the host from subsequent infection. The underlying pathways controlling the maintenance of memory CD4+ T cells remain undefined. Memory CD4+ T cell survival is impaired in the absence of the Notch signaling protein known as recombination signal binding protein for immunoglobulin k J region (Rbpj). Rbpj-deficient CD4+ memory T cells exhibit reduced glucose uptake due to impaired Akt phosphorylation, resulting in low Glut1 expression. Together, these data define a central role for Notch signaling in maintaining memory CD4+ T cells through the regulation of glucose uptake.

Free Research Field

免疫学、寄生虫学