With no variable effect on ROS generation (S1F and S1G Fig), BBR treatment significantly induced apoptosis in uninfected (S1H Fig) and M. tb infected macrophages (Fig 1B and 1C) and led to significant activation of transcription factors (NFkB and STAT3) which play a crucial role in combating TB (Fig 1D). Further, BBR treatment significantly enhanced the expression of CD11b and co-stimulatory molecules CD40 and CD86 on the surface of infected macrophages (Fig 1E–1G). This evidence concerns the gene CD86 and tuberculosis.