Inflammatory monocytes contribute to the persistence of CXCR3 CX3CR1 circulating and lung-resident memory CD8 T cells following respiratory virus infection.

Phenotypically diverse memory CD8 T cells are present in the lungs that either re-circulate or reside within the tissue. Understanding the key cellular interactions that regulate the generation and then persistence of these different subsets is of great interest. Recently, DNGR-1 dendritic cell (DC) mediated priming was reported to control the generation of lung-resident but not circulating memory cells following respiratory viral infection. Here, we report an important role for Ly6C inflammatory monocytes (IMs) in contributing to the persistence of memory CD8 T cells but not their generation. Effector CD8 T cells expanded and contracted normally in the absence of IMs, but the memory compartment declined significantly over time. Quite unexpectedly, this defect was confined to tissue resident and circulating CXCR3 CX3CR1 memory cells but not CXCR3 CX3CR1 and CXCR3 CX3CR1 subsets. Thus, two developmentally distinct innate cells orchestrate the generation and persistence of memory T cell subsets following a respiratory virus infection. See also: News and Commentary by Lafouresse & Groom.