Persistence in Temporary Lung Niches: A Survival Strategy of Lung-Resident Memory CD8(+) T Cells

Takamura, Shiki

CCR7 is also known to regulate the egress of effector CD8 + cells from the lung interstitium through the lymph (12, 19, 56) . This is consistent with the fact that activated respiratory DCs migrate to the MLN in a CCR7-dependent manner (39, 42) . As is the case with S1P 1 , antigen recognition in the lung leads to downregulation of CCR7 on effector CD8 + T cells, suggesting that S1P 1 and CCR7 cooperatively accelerate the egress of antigen-specific CD8 + T cells from the lung. It is also noteworthy that antigen-dependent selective retention of effector CD8 + T cells may prevent overt pathogenesis by decreasing the number of bystander T cells at the site of infection (56) . However, as most CCR7 should be already downregulated when expanded effector CD8 + T cells leave the MLN and all of previous data were analyzed in the presence of large proportions of cell contaminants in the blood, analysis using i.v. staining would be required to precisely understand the role of this chemokine receptor.