Mycobacterium tuberculosis remains one of the world’s most deadly bacteria resulting in infection in nearly a third of the global population and millions of deaths per year. Recent advances in our understanding of tuberculosis infection demonstrate that infection within a given individual is highly heterogeneous; however, the determinants that drive lesions towards complete bacterial sterilization remain poorly understood.    Our lab is interested in developing new tools and paradigms to dissect the complex dynamics of bacterial infection.  We work at a variety of biological scales ranging from single cells to infected animals sitting in both “reference frames” by taking both an immunologist’s and a microbiologist's perspective. Combining new technologies with classical approaches and quantitative modeling, we plan to apply our findings to modulating macrophage function in disease with the goal of reverse-engineering a vaccine for tuberculosis.   Two motivating questions in the lab currently include:   (1) What macrophage processes contribute to effective bacterial killing and what are the bacterial evasion mechanisms to resist such stress?   (2) How can manipulate macrophage plasticity and program macrophage function in homeostasis and disease?