| Project/Area Number |
24689043
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| Research Category |
Grant-in-Aid for Young Scientists (A)
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| Allocation Type | Partial Multi-year Fund |
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| Research Field |
Infectious disease medicine
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| Research Institution | Kinki University |
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Principal Investigator |
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| Project Period (FY) |
2012-04-01 – 2014-03-31
|
| Project Status |
Completed (Fiscal Year 2013)
|
| Budget Amount *help |
¥18,460,000 (Direct Cost: ¥14,200,000、Indirect Cost: ¥4,260,000)
Fiscal Year 2013: ¥6,110,000 (Direct Cost: ¥4,700,000、Indirect Cost: ¥1,410,000)
Fiscal Year 2012: ¥12,350,000 (Direct Cost: ¥9,500,000、Indirect Cost: ¥2,850,000)
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| Keywords | 感染防御学 / メモリーCD8T細胞 / 肺粘膜 / 感染症防御学 |
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| Research Abstract |
Memory CD8+ T cells in the lung airways are maintained by a process of continual recruitment. However, the mechanisms by which Memory CD8+ T cells are recruited to the lung airways during steady-states are poorly understood. Here we show that sphingosine-1-phosphate receptor 1 (S1P1) regulates memory CD8+ T-cell egress from the lung parenchyma, while chemokine receptor CXCR6 promotes continuous migration toward CXCL16 gradient to the lung airways. CD69 upregulated on memory CD8+ T cells upon reactivation in the lung parenchyma inhibited S1P1, thereby preventing egress from this tissue. Furthermore, CXCR6 is also upregulated upon reactivation, which reinforces migration to the lung airways. Such reactivation-associated factors cooperatively enable memory CD8+ T cells to be recruited to the lung airways. These findings highlight a unique continuous developmental process of tissue resident memory (TRM) cells in the lung airways, and a crucial role of CD69 in this process.
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