HVEM imprints memory potential on effector CD8 T cells required for protective mucosal immunity

Pritesh Desai, Georges Abboud, Jessica Stanfield, Paul G. Thomas, Jianxun Song, Carl F. Ware, Michael Croft, Shahram Salek-Ardakani

Research output: Contribution to journalArticlepeer-review

17 Scopus citations


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 shortlived 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.

Original languageEnglish (US)
Pages (from-to)2968-2975
Number of pages8
JournalJournal of Immunology
Issue number8
StatePublished - Oct 15 2017

All Science Journal Classification (ASJC) codes

  • Immunology and Allergy
  • Immunology


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