Elucidating the molecular basis of memory CD8+ T cell maintenance

2015 Fiscal Year Final Research Report

• Project/Area Number: 26860325
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Immunology
• Research Institution: Kyoto University
• Principal Investigator: Setoguchi Ruka 京都大学, 医学(系)研究科(研究院), 准教授 (50415204)
• Project Period (FY): 2014-04-01 – 2016-03-31
• Keywords: 免疫記憶 / 恒常性維持 / MHCクラスII

Outline of Final Research Achievements

Memory CD8 T cells are long-lived antigen (Ag)-specific T cells which respond quickly and exert effector functions faster than naive T cells upon reencounter with the Ags. Memory CD8 T cells are maintained at a stable size over long periods, but the mechanisms by which their size is maintained remain elusive. It has been proposed that the maintenance of memory CD8 T cells depends on CD4 T cells, based on the observation that CD8 T cells which have been primed with Ags in wild-type (WT) mice survive poorly when transferred into MHCII-/- as compared to WT hosts. Our study revealed that the impaired maintenance of memory CD8 T cells in MHCII-/- mice is not due to the absence of CD4 T cells. Our RNA-Seq analysis showed the upregulation of effector-like gene expressions in memory CD8 T cells in MHCII-/- compared with in WT mice. Antibiotics treatment or Myd88 deficiency did not alter the defect, indicating that commensal bacteria or Myd88-dependent signal was not involved with the defect.

Free Research Field

免疫学