Journal
JOURNAL OF INFECTIOUS DISEASES
Volume 202, Issue 4, Pages 524-532Publisher
OXFORD UNIV PRESS INC
DOI: 10.1086/654932
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Funding
- National Agency for Promotion of Science and Technology (ANPCyT) [PICT 25996, PICT 2332, PICT 01384]
- National Council of Science and Technology (CONICET) [PIP 5584]
- University of Buenos Aires [UBACyT X087]
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Tuberculous pleurisy allows the study of specific cells at the site of Mycobacterium tuberculosis infection. Among pleural lymphocytes, natural killer (NK) cells are a major source of interferon gamma (IFN-gamma), and their functions are regulated by activating and inhibitory receptors. Programmed death-1 (PD-1), programmed death ligand 1 (PD-L1), and programmed death ligand 2 (PD-L2) are recognized inhibitory receptors in adaptive immunity, but their role during innate immunity remains poorly understood. We investigated the PD-1: PD-L1/PD-L2 pathway on NK cell effector functions in peripheral blood and pleural fluid from patients with tuberculosis. M. tuberculosis stimulation significantly up-regulated PD-1, PD-L1, and PD-L2 levels on NK cells. Interestingly, a direct correlation between PD-1 and IFN-gamma expression on NK cells was observed. Moreover, blockade of the PD-1 pathway markedly augmented lytic degranulation and IFN-gamma production of NK cells against M. tuberculosis. Furthermore, PD-1(+) NK cells displayed a diminished IFN-gamma mean fluorescence intensity, denoting the relevance of PD-1 on IFN-gamma regulation. Together, we described a novel inhibitory role played by PD-1: PD-L interactions in innate immunity in tuberculosis.
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