| First Author | Desai P | Year | 2017 |
| Journal | J Immunol | Volume | 199 |
| Issue | 8 | Pages | 2968-2975 |
| PubMed ID | 28864473 | Mgi Jnum | J:251261 |
| Mgi Id | MGI:6103389 | Doi | 10.4049/jimmunol.1700959 |
| Citation | Desai P, et al. (2017) HVEM Imprints Memory Potential on Effector CD8 T Cells Required for Protective Mucosal Immunity. J Immunol 199(8):2968-2975 |
| abstractText | 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. |
