Genetic absence of PD-L1 does not restore CD8⁺ T cell function during respiratory virus infection and delays virus clearance.

ABSTRACT: A key mediator of T cell impairment during respiratory virus infection is the inhibitory receptor PD-1. PD-1 is induced on T cells following antigen exposure, whereas proinflammatory cytokines upregulate the ligands PD-L1 and PD-L2. Respiratory virus infection leads to upregulation of PD-L1 on airway epithelial cells, dendritic cells, and alveolar macrophages. However, the role of PD-L1 on different cell types in acute respiratory virus infections is not known. We sought to determine the role of PD-L1 on different cell types in CD8⁺ T cell impairment. We found that PD-L1^-/- mice challenged with human metapneumovirus or influenza showed a similar level of CD8⁺ T cell impairment compared to wild-type (WT) mice. Moreover, virus clearance was delayed in PD-L1

SUBMITTER: Rogers MC 

PROVIDER: S-EPMC11495042 | biostudies-literature | 2024 Oct

REPOSITORIES: biostudies-literature