Mycobacterium tuberculosis interferes with the ability of its host cell to undergo apoptosis. Arnett et al. report that the pathogen promotes macrophage survival by engaging the nuclear receptor PPARγ to induce the antiapoptotic protein MCL-1, yielding insights into the pathogenesis of tuberculosis and potentially unlocking new avenues for therapeutic intervention.
Keywords: MCL-1; PPARγ; apoptosis; host-directed therapy; tuberculosis.
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