Assessment the Diversity of Circulating Natural Killer Cells Between Active Tuberculosis and Latent Tuberculosis Infection

Abstract Background: Tuberculosis (TB) is a leading global public health problem, but the mechanisms underlying the immunopathology of TB progression are not well understood. It is currently believed that Mycobacterium tuberculosis (Mtb) infection can modify NK cell phenotypic signatures. Hence, our study was designed to investigate the diversity of circulating NK cells between active TB and latent TB infection. Peripheral blood NK subsets, as well as their expression of activating and inhibitory membrane receptors in different TB-infected status were evaluated in the present study. Results : Significant differences of NK phenotypes were observed in the ATB, LTBI and HC populations. Among them, CD56 Bright CD16 Dim ( P ATB VS HC =0.008, P LTBI VS HC =0.017) and CD27+CD56 Bright CD16 Dim ( P ATB VS HC =0.022, P LTBI VS HC =0.004) NK subsets were increased in TB-infected groups compared with HC group. On the contrary, the proportion of CD27 in NK cells ( P ATB VS HC =0.036, P LTBI VS HC =0.006) and CD56 Dim CD16+ NK subsets ( P ATB VS HC =0.0001, P LTBI VS HC =0.001) were diminished in TB-infected groups. Furthermore, the proportion of KLRG1 in NK cells ( P =0.036), as well as their subsets CD56 Dim CD16+ NK ( P =0.046) and CD27+ NK ( P =0.027), were increased significantly in LTBI compared with the ATB group; while Mtb specific IFN-γ+CD56 Bright CD16 Dim NK cells expressed higher KLRG1 in ATB than LTBI ( P =0.027). Within CD56 Bright CD16 Dim NK subsets, the percentage of KLRG1 was elevated in ATB patients compared with HC group ( P =0.037). However, the expression of activating receptor NKG2D in NK and its subsets showed no significant between the three participant groups. Conclusions: The present results demonstrated that the different TB infection states were coupled with the diversity of NK cell compartments, and the expression of KLRG1 in NK cells might be a specific phenotype to modulate the progression of TB from latent to active.