I began my scientific training at the University of California, San Francisco, studying the initiation of the adaptive immune response to Mycobacterium tuberculosis with Dr. Joel D. Ernst. My thesis research focused on developing methods of quantitating and characterizing the subsets of phagocytes that are infected by M. tuberculosis in the lung and lymph node during the course of infection, followed by an examination of how the delay in movement of infected cells to the draining lymph node contributes to delayed onset of the adaptive immune response and chronic nature of the M. tuberculosis infection. After graduate school, I joined the laboratory of Dr. David Underhill at Cedars-Sinai to gain experience studying the innate inflammatory responses of phagocytes in response to bacteria and fungi. I studied the importance of dectin-1 and caspase recruitment domain-containing protein 9 (CARD9) to the antifungal immune responses as well as how human polymorphisms in dectin-1 and CARD9 impact disease. I also studied the activation of the innate immune-signaling complex, the NLRP3 inflammasome, in response to bacterial cell wall peptidoglycan. As an assistant professor, my laboratory focuses on how degradation of bacteria and fungi by phagocytes alters the inflammatory responses and the metabolism of the phagocytes. The crosstalk between the innate immune system of the cell and the metabolism of the phagocytes determines the degree and duration of the inflammatory signals. We are studying the importance of the glycolytic enzyme hexokinase to sensing bacteria and inflammatory sugars generated during degradation of cell wall peptidoglycan. In addition, the laboratory is studying the importance of the multiple hexokinase genes expressed by phagocytes to the regulation of their inflammatory responses during bacterial infection and during inflammatory diseases such as inflammatory bowel disease.