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. 2010 Aug 15;202(4):524-32.
doi: 10.1086/654932.

Role played by the programmed death-1-programmed death ligand pathway during innate immunity against Mycobacterium tuberculosis

Ivana B Alvarez  1 , Virginia Pasquinelli, Javier O Jurado, Eduardo Abbate, Rosa M Musella, Silvia S de la Barrera, Verónica E García
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Role played by the programmed death-1-programmed death ligand pathway during innate immunity against Mycobacterium tuberculosis

Ivana B Alvarez et al. J Infect Dis. .

Abstract

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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