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Mycobacterium tuberculosis , the bacterium that causes tuberculosis, is one of the most successful pathogens of humans. It has evolved several adaptive skills and evasion mechanisms to hijack the immunologically educated host to suit its intracellular lifestyle. Here, we show that one of the unique PPE family member proteins of  M. tuberculosis , PPE2, can limit nitric oxide (NO) production by inhibiting  inos  gene transcription. PPE2 protein has a leucine zipper DNA-binding motif and a functional nuclear localization signal. PPE2 was translocated into the macrophage nucleus  via  the classical importin α/β pathway where it interacted with a GATA-binding site overlapping with the TATA box of  inos  promoter and inhibited NO production. PPE2 prolonged intracellular survival of a surrogate bacterium  M. smegmatis in vitro  as well as  in vivo . This information are likely to improve our knowledge of host-pathogen interactions during  M. tuberculosis  infection which is crucial for designing effective anti-TB therapeutics.

The PPE2 protein of Mycobacterium tuberculosis translocates to host nucleus and inhibits nitric oxide production