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In the Stallings Laboratory, we dissect the molecular details of Mycobacterium tuberculosis pathogenesis, from the perspective of both the host and the pathogen. We use a combination of genetics, biochemistry, cell biology, and animal models of disease to seek better understanding of how M. tuberculosis defends itself against host immune attacks and antibiotic therapy as well as what immune responses are required to control M. tuberculosis infection. We have identified a number of mycobacterial proteins that function as mediators of mycobacterial stress responses and are required for pathogenesis. In particular, we are currently focusing on how regulation of gene expression, DNA replication, and respiration allow M. tuberculosis to adapt to host-derived stresses and antibiotic therapy. In addition, we have discovered multiple host proteins and immune pathways that are required to control M. tuberculosis infection and prevent active tuberculosis disease. In particular, our studies highlight the importance of the innate immune response in regulating neutrophil-predominated inflammation to prevent tissue damage. In addition to these mechanistic studies, the lab is working to apply our basic science findings to the treatment of disease in humans.