I am an infectious diseases physician-scientist and Assistant Professor of Medicine, Microbiology and Immunology at the Renaissance School of Medicine at Stony Brook University, where I started my independent laboratory in 2021.  I have extensive experience in clinical and translational Tuberculosis research and my current work focuses on innate lymphocyte immunity during Mycobacterium tuberculosis (Mtb) infection.  Tuberculosis (TB) remains a leading cause of global mortality, yet the immune mechanisms underlying innate resistance or susceptibility to infection remain poorly understood.  To definitively control the epidemic, fundamental questions of host immunity must be answered, namely (1) why do some individuals highly exposed to Mtb develop infection, while others with similar intensity of exposure, remain uninfected?  and (2) How do those who develop asymptomatic infection maintain latency or progress to active disease?  For the past 10 years, we have studied innate-like T cells that express highly conserved T cell receptors recognizing non-peptide microbial ligands during Mtb infection.  These cells can execute rapid responses at mucosal surfaces and potentially sterilize infection.  In our published work, we interrogated a cohort of recently exposed household contacts of active TB patients in Haiti and discovered that both MAIT and  gd T cells respond to recent tuberculosis infection.  Further, we showed that MR1 ligand vaccination resulting in robust enrichment of MAIT cell numbers in murine lung alone was not sufficient to protect against infection.  We performed single cell RNA sequencing (scRNAseq) of human MAIT cells in unexposed healthy donors and observed heterogeneous CD4+/CD8+ subsets with divergent transcriptional signatures, including a novel FOXP3+ subset that resembles Treg cells. Importantly, we found that these subsets were also detectable during recent Mtb exposure and infection.  Recent work in IV BCG vaccinated macaques demonstrates that CD8aa lymphocytes are critical to protection against primary Mtb infection and that a significant proportion of these cells are MAIT cells and NK cells, two subsets upon which our laboratory has focused its investigation since founding in 2021. In our most recent work we discovered that TRAV1-2 negative CD4+ MAIT cells have unexpectedly high TCR diversity. These cells also significantly expand in long-term TB resistors. Our ongoing work seeks to test the hypothesis that non-canonical TRAV1-2 negative MAIT cells are selected by natural human infection using unique cohorts of household contacts, active TB patients and source community controls. We also hypothesize that CD4+ TRAV1-2 negative cells respond to distinct ligand classes in addition to riboflavin intermediates that we seek to identify using human platform MR1 purification systems. Our overarching goal is to apply these systems immunology approaches to develop immune-targeted therapy against tuberculosis and other human pathology.