HVEM Imprints Memory Potential on Effector CD8 T Cells Required for Protective Mucosal Immunity.

Abstract

Mucosal immunity to reinfection with a highly virulent virus requires the accumulation and persistence of memory CD8 T cells at the site of primary infection. These cells may derive from memory precursor effector cells (MPECs), which are distinct from short-lived effector cells that provide acute protection but are often destined to die. Using respiratory virus infection, we show that herpes virus entry mediator (HVEM; TNFRSF14), a member of the TNF receptor superfamily, provides key signals for MPEC persistence. HVEM-deficient CD8 T cells expanded normally but were skewed away from MPECs with resultant poor development of circulating and lung-resident memory cells. HVEM was selectively expressed on MPECs whereas MPECs deficient in HVEM failed to survive in adoptive transfer recipients. As a consequence, HVEM-deficient recipients failed to afford protection against respiratory reinfection with influenza virus. HVEM therefore represents a critical signal for MPECs and development of protective mucosal CD8 T cell memory.

DOI: 10.4049/jimmunol.1700959

Cite this paper

@article{Desai2017HVEMIM, title={HVEM Imprints Memory Potential on Effector CD8 T Cells Required for Protective Mucosal Immunity.}, author={Pritesh Desai and Georges Abboud and Jessica Stanfield and Paul G Thomas and Jianxun Song and Carl F Ware and Michael Croft and Shahram Salek-Ardakani}, journal={Journal of immunology}, year={2017}, volume={199 8}, pages={2968-2975} }