Abstract
Induction of memory CD8 T cells residing in peripheral tissues is of interest for T cell-based vaccines as these cells are located at mucosal and barrier sites and can immediately exert effector functions, thus providing protection in case of local pathogen encounter. Different memory CD8 T cell subsets patrol peripheral tissues, but it is unclear which subset is superior in providing protection upon secondary infections. We used influenza virus to induce predominantly tissue resident memory T cells or cytomegalovirus to elicit a large pool of effector-like memory cells in the lungs and determined their early protective capacity and mechanism of reactivation. Both memory CD8 T cell pools have unique characteristics with respect to their phenotype, localization, and maintenance. However, these distinct features do not translate into different capacities to control a respiratory vaccinia virus challenge in an antigen-specific manner, although differential activation mechanisms are utilized. 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 in an antigen-independent and partially chemokine-driven manner. Together these results bear relevance for the development of vaccines aimed at eliciting a protective memory CD8 T cell pool at mucosal sites.
Highlights
CD8 T cells are activated in an antigen-specific manner and have the ability to eliminate pathogens by producing effector cytokines and exerting cytotoxic functions
We focused on the lungs as both Tissue resident memory (TRM) cells and MCMV-induced inflationary T cells are established in this tissue.[30,31,32]
A higher proliferative capacity was found in memory T cells induced by influenza virus infection. These results suggest that the increased number of OVA-specific CD8 T cells in the MCMVsetting after local vaccinia virus (VV)-OVA challenge might be primarily due to relocation of circulating cells to the lung tissue
Summary
CD8 T cells are activated in an antigen-specific manner and have the ability to eliminate pathogens by producing effector cytokines and exerting cytotoxic functions. A small population of T cells persists as memory cells that have the capacity to respond and rapidly expand upon secondary antigen encounter. Effector memory T cells (TEM) mainly recirculate and do not express lymphoid tissue homing molecules One hallmark of these cells is their robust effector functions. Antigen first has to be transported to the lymphoid tissues where it is presented by professional antigen presenting cells to T cell zone-homing and resident TCM cells It is not entirely clear how TEM cells are reactivated, but there is evidence that the size of the TEM pool in peripheral tissues and blood is directly linked to its early protective capacity,[2,3,4] indicating that these cells respond directly in the infected tissue
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
