How distinct virus-specific memory CD8 T cell subsets control respiratory virus infection

Cytomegalovirus infection induces large numbers of circulating memory CD8 T cells, while influenza virus infection induces tissue-resident memory CD8 T cells in the lung. A recent ‘Mucosal Immunology’ paper by the Oxenius group shows that both subsets equally protect against respiratory infection, albeit employing different mechanisms of activation and relocation.

Graphical abstract Welten paper
Protective capacity of influenza A virus-induced TRM cells and MCMV-induced inflationary CD8 T cells in the lung tissue

Induction of memory CD8 T cells residing in peripheral tissues is of interest for T cell-based vaccines as these cells can immediately exert effector functions providing protection in case of local pathogen encounter. Different memory CD8 T cell subsets are present in peripheral tissues, but it is unclear which subset is superior in providing protection. We used influenza virus to induce predominantly tissue resident memory T cells or cytomegalovirus (MCMV) to elicit a large pool of effector-like memory cells in the lungs and determined their early protective capacity and mechanism of reactivation. Despite their different phenotype and localization in lung tissue, both memory CD8 T cell subsets provided comparable protection against a respiratory infection. While influenza-induced memory CD8 T cells respond to antigen by local proliferation, MCMV-induced memory CD8 T cells relocate from the vasculature into the tissue. Together these results bear relevance for the development of vaccines aimed at eliciting a protective memory CD8 T cell pool at mucosal sites.

Link to the publication in external page "Mucosal Immunology".

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