Recent advances have provided substantial insight into the maintenance of mucosal immunity and the 
pathogenesis of inflammatory bowel disease. Cellular programs responsible for intestinal homeostasis 
use diverse intracellular and intercellular networks to promote immune tolerance, inflammation or 
epithelial restitution. Complex interfaces integrate local host and microbial signals to activate 
appropriate effector programs selectively and even drive plasticity between these programs. In 
addition, genetic studies and mouse models have emphasized the role of genetic predispositions and 
how they affect interactions with microbial and environmental factors, leading to pro-colitogenic 
perturbations of the host-commensal relationship.