My lab’s long-term objective is to uncover novel mechanisms underlying the pathology of Crohn’s disease (CD), a progressive uncurable disease characterized by transmural intestinal inflammation leading to complications often requiring bowel resection surgery. The goal is to identify novel therapeutic targets by focusing on two previously disconnected hallmarks of CD: expanded mesenteric adipose tissue wrapping around the intestine – or creeping fat – and anti-microbial antibodies, both correlating with disease complications.

Studying these hallmarks will further reveal unexplored relationships between adipocytes, stromal cells and immune cells driving B cell responses in gut homeostasis and inflammation. Understanding these relationships will impact how we perceive immune responses at other mucosal sites and systemically. Ongoing projects include: the study of the impact of CD-specific microbiota on stromal cell-supported lymphoid structures embedded in mesenteric adipose tissue; specific mechanisms by which stromal cells and adipocytes communicate with B cells; and the subsequent impact on B cell activation and their differentiation to anti-microbial antibody-producing plasma cells. Future projects will investigate how these relationships are established in early life and evolve overtime.