Abstract
Inflammatory bowel disease (IBD), encompassing Crohn's disease (CD) and ulcerative colitis (UC), is a chronic inflammatory disorder caused by dysregulated immune responses in a genetically predisposed individual. Recent accumulating data, including genome-wide association studies, have identified more than 50 distinct genetic loci that confer susceptibility. We highlight the role of microbial-host interaction, particularly with respect to the overlap of common genetic and pathophysiologic mechanisms of CD and UC, interleukin-22-producing natural killer cells, autophagy, and TL1A, a member of the tumor necrosis factor (TNF) family, in gut homeostasis and IBD pathogenesis. This article focuses on the recent advances in understanding of IBD from the past year, including advances in genetics and immunobiology.