Dr. Philpott’s laboratory investigates the molecular and cellular mechanisms of innate immunity with a focus on the NOD-like receptor (NLR) family and their roles in shaping host defense, intestinal immune homeostasis, and disease pathogenesis. His research integrates gnotobiotic, conventional, and human-microbiota–associated murine models to dissect host–microbe interactions in the gastrointestinal tract. A significant emphasis is placed on Crohn’s disease (CD)-associated susceptibility genes, including NOD2 and ATG16L1, to elucidate how these pathways regulate bacterial autophagy, immune signaling, and when dysfunctional, chronic intestinal inflammation. In collaboration with Dr Stephen Girardin, Dr. Philpott’s early contributions defined the bacterial ligands for NOD1 and NOD2 and demonstrated how their interaction with ATG16L1 influences antibacterial autophagy, thereby linking innate immune pathways to CD pathogenesis. Collectively, Dr. Philpott’s studies aim to advance mechanistic understanding of how innate immunity and the microbiota drive inflammatory bowel disease.