Figure 3. Model of PD-1 activity and therapeutic intervention.
Chronic stimulation of antigen presenting cells (APC) by HIV induces high expression of PD-L1 on the APC, and strong expression of PD-1 on responding CTL. Negative signaling through PD-1 in association with the peptide/MHC–TCR interaction leads to decreased proliferation and increased apoptosis of HIV-specific CTL. Anti-PD-1 therapy could block the negative regulatory signal through PD-1 thereby restoring proliferative potential in HIV-specific CTL despite the high expression of PD-1.