LCMV induced downregulation of HVEM on antiviral T cells is critical for an efficient effector response.

ABSTRACT: T-cell responses against tumors and pathogens are critically shaped by cosignaling molecules providing a second signal. Interaction of herpes virus entry mediator (HVEM, CD270, TNFRSF14) with multiple ligands has been proposed to promote or inhibit T-cell responses and inflammation, dependent on the context. In this study, we show that absence of HVEM did neither affect generation of effector nor maintenance of memory antiviral T cells and accordingly viral clearance upon acute and chronic lymphocytic choriomeningitis virus (LCMV) infection, due to potent HVEM downregulation during infection. Notably, overexpression of HVEM on virus-specific CD8⁺ T cells resulted in a reduction of effector cells, whereas numbers of memory cells were increased. Overall, this study indicates that

SUBMITTER: Diethelm P 

PROVIDER: S-EPMC9321772 | biostudies-literature | 2022 Jun

REPOSITORIES: biostudies-literature