Elucidating the molecular basis of memory CD8+ T cell maintenance
| Project/Area Number |
26860325
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Immunology
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| Research Institution | Kyoto University |
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Principal Investigator |
Setoguchi Ruka 京都大学, 医学(系)研究科(研究院), 准教授 (50415204)
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| Project Period (FY) |
2014-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 免疫記憶 / 恒常性維持 / MHCクラスII / 免疫学的記憶 |
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| 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.
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Report
(3 results)
Research Products
(3 results)
