CD69 and CD103 cooperatively regulate CD8 T cell responses in the lungs after viral infection (39.25)

Abstract

Abstract T cell mediated immunity to influenza infection disappears within a few months, even though large numbers of virus-specific memory CD8 T cells remain in the circulation for at least two years. It has been suggested that antigen persistence may play an instrumental role in protective cellular immunity. This idea is supported by the presence of activated virus-specific CD8 T cells in the respiratory tract during the months following infection, when processed influenza antigens are presented to virus-specific CD8 T cells in the draining lymph nodes. A majority of the endogenous virus-specific CD8 T cells that were at the mucosal surface of the lungs one month after infection expressed both CD69 and CD103. In contrast, bystander memory CD8 T cells that entered the lungs during parabiosis did not acquire this phenotype. We have crossed CD69KO and CD103KO mice with F5 TcR transgenic mice which are specific for the influenza NP peptide. Transfer studies show that CD103-deficiency results in reduced numbers of CD69+ NP-specific CD8 T cells in the lungs. In contrast, CD69-deficiency results in slightly delayed T cell activation followed by a late accumulation of CD103-negative NP-specific CD8 T cells in the lung parenchyma. This work was supported by NIH grants AI065895 & AI071213 (LSC), RO1 AI-36532 (GH).