The dysregulation of immune cells known as macrophages is a hallmark of diseases in which chronic inflammation is known to play a role, including cancer, atherosclerosis, and obesity/type 2 diabetes. Because macrophages are highly influenced by their environment, we need to understand how disease-specific changes to their environment alter specific biochemical and genetic pathways to drive pathogenesis. Moreover, the relationship of these macrophage pathways to those required for their role in clearing pathogens is largely unknown. This is important because attempts to therapeutically target macrophages must preserve this important function of theirs. Comparing and contrasting macrophages across a spectrum of diseases is essential to elucidating disease-specific mechanisms and developing therapeutics that are both efficacious and safe. To enable this, my lab combines proteomic, bioinformatic, immunologic, and functional approaches to study macrophages in an unbiased manner across a spectrum of diseases. Our long-term goal is to develop a robust research program that uses a multi-disease approach to develop a comprehensive understanding of macrophage biology, and then translates this mechanistic understanding to develop therapeutics across a spectrum of human disease. To that end, my lab is developing two new therapies for the treatment of many cancers, and anti-inflammatory therapies that do not interfere with pathogen clearance for treating atherosclerosis and type 2 diabetes.

I am currently an associate professor at the Ben May Department for Cancer Research at the University of Chicago and have received the J Clifford Moos Award for Cancer Research (2017- 2020) and the Young Investigator Award of the Cancer Research Foundation (2014-2016).