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The role of the PD-1/PD-L pathway in a murine model of tuberculosis remains controversial regarding viral infections and clinical tuberculosis. We conducted a case-control study to investigate the modulating role and mechanism of the PD-1/PD-L pathway in patients with active tuberculosis. Fifty-nine participants, including 43 active tuberculosis (ATB) patients and 16 healthy controls (HC), were enrolled. Cell surface staining and flow cytometry were used to detect the expressions of PD-1 and its ligands on T cells and monocytes. Intracellular cytokine staining was used to determine the PPD-specific IFN-γ-secreting T-cell proportion. CD4 +  T-cell proliferation and macrophage functions were investigated in the presence or absence of PD-1/PD-L pathway blockade. Proportions of both PD-1 + CD4 +  and PD-L1 + CD4 +  T cells in ATB patients were more significantly increased than in the HC group ( P  = 0.0112 and  P  = 0.0141, respectively). The expressions of PD-1, PD-L1, and PD-L2 on CD14 +  monocytes in ATB patients were much higher than those in the HC group ( P  = 0.0016,  P  = 0.0001, and  P  = 0.0088, respectively). Blockade of PD-1 could significantly enhance CD4 +  T-cell proliferation ( P  = 0.0433). Phagocytosis and intracellular killing activity of macrophages increased significantly with PD-1/PD-L pathway blockade. In conclusion, the PD-1/PD-L pathway inhibits not only  M . tb -specific CD4 +  T-cell-mediated immunity but also innate immunity.

PD-1/PD-L pathway inhibits M.tb-specific CD4+ T-cell functions and phagocytosis of macrophages in active tuberculosis