Data from the mechanistic experiments suggest that phosphoantigen/IL2-expanded Vγ2Vδ2 T effector cells producing granulysin/perforin during Mtb infection may contribute to the in vivo function restricting Mtb infection or dissemination while these expanded γδ T cells are actively mounting anti-TB Th1-like IFNγ cellular responses. Here, PRF1 is linked to tuberculosis.