Fig. 1.

The role of T cells in the antiviral defense and pulmonary immunopathology. a) CD8 T cell-mediated response develops after primary RSV infection. Viral antigens are presented by the antigen-presenting cells (APCs), most commonly, by DCs. Naïve CD8 T cells (naive CD8 T) become activated and differentiate into RSV-specific CD8 T cells (RSV-CD8 T), which then proliferate peaking on days 8-10 post-infection. RSV-CD8 T cells produce large amounts of pro-inflammatory cytokines IFNγ and TNFα, which mediate pulmonary immunopathology. After reaching the plateau, the number of RSV-CD8 T cells declines and they give rise to the memory T cells represented by several phenotypic subsets: 1) T_CM – central memory T cells (CD62L^hi/CCR7^hi/IL-7Rα^hi/KLRG1^l°) circulate in the bloodstream and accumulate in the secondary lymphoid tissues; 2) T_EM – effector memory T cells (CD62L^l°/CCR7^l°/IL-7Rα^l°/KLRG1^hi) are mainly located in the lungs, but can circulate in the bloodstream; 3) T_RM – tissue-resident memory T cells (CD62L^l°/CD69^hi/CD103^hi) are found solely in the lungs and are unable to exit into the circulation. b) T_EM and T_RM exert protective antiviral response by triggering apoptosis and direct lysis of infected cells.