SWAG��Ƶ

My laboratory focuses on neuro-immune cell interactions in chronic and neuropathic pain syndromes, specifically studying how T cells impact neuronal responses properties. Skilled in multi-color flow cytometry,  multi-analyte assays, 2D DiGE and 2D Western, phospho-profiling, and mouse behavioral models (Hargreaves, von Frey, thermal choice assay). I earned my Doctor of Philosophy (Ph.D.) in Immunology from The Johns Hopkins University, and received training at the National Institutes of Health, Yale University, and Population Council. I have 5 years' experience (4yrs graduate, 1yr undergraduate) teaching immunology and microbiology in both a standard classroom and an integrated medical school curriculum coupled with flipped learning. 

In 2008 at the National Institutes of Health, I discovered that the HIV envelope protein gp120 binds to integrin α4β7, the gut homing receptor. Expression of integrin α4β7 mediates migration of T cells to the gut where massive CD4+ T cells depletion occurs and subsequent HIV-induced immune dysfunction. We later showed that integrin α4β7 forms a complex with CD4 and defines a T cell subset that is highly susceptible to HIV infection. 

In 2014 as a post-doctoral fellow at Population Council, we showed that HSV-2 infection increased the frequency of α4β7+ T cells in the rectal and vaginal mucosa. This increased expression directly correlated with the increased susceptibility to Simian-Human Immunodeficiency virus (SHIV) infection. These experiments highlighted α4β7 as an important risk factor for HIV transmission. Additionally, we analyzed the effect that sex hormones had on α4β7+ T cells and the mucosal microenvironment. Progesterone and estradiol modified the expression and release of inflammatory immune factors directly implicated in HIV transmission. These experiments underscore the importance of understanding the hormone-driven modulation of the mucosal microenvironment and the implementation of contraceptive polices in high-risk communities.

In 2017 as a post-doctoral fellow at the SWAG��Ƶ, my research focused on the roles of exchange proteins activated by cAMP (Epac) signaling pathways in primary sensory neurons and the contribution to the development of acute pain. Our work identified a previously unknown pathway by which tissue injury increases pain by enhancing mitochondrial function through the phosphorylation of the enzyme pyruvate dehydrogenase (Pdha1). An exciting observation is that this mitochondrial mechanism only occurs in male mice, not females, suggesting the need for sex-specific treatments.