HVEM Imprints Memory Potential on Effector CD8 T Cells Required for Protective Mucosal Immunity. Academic Article uri icon

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.

altmetric score

  • 1.75

author list (cited authors)

  • Desai, P., Abboud, G., Stanfield, J., Thomas, P. G., Song, J., Ware, C. F., Croft, M., & Salek-Ardakani, S.

citation count

  • 10

publication date

  • October 2017