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The engagement of programmed death 1 (PD-1) to its ligands, PD-L1 and PD-L2^,,,, inhibits proliferation and cytokine production mediated by antibodies to CD3 (refs. ,,). Blocking the PD-1–PD-L1 pathway in mice chronically infected with lymphocytic choriomeningitis virus restores the capacity of exhausted CD8⁺ T cells to undergo proliferation, cytokine production and cytotoxic activity and, consequently, results in reduced viral load. During chronic HIV infection, HIV-specific CD8⁺ T cells are functionally impaired^,,, showing a reduced capacity to produce cytokines and effector molecules as well as an impaired capacity to proliferate^,,,. Here, we found that PD-1 was upregulated on HIV-specific CD8⁺ T cells; PD-1 expression levels were significantly correlated both with viral load and with the reduced capacity for cytokine production and proliferation of HIV-specific CD8⁺ T cells. Notably, cytomegalovirus (CMV …