The inflammatory bowel diseases (IBDs), Crohn's disease and ulcerative colitis, are chronic inflammatory disorders caused by dysregulated immune responses in genetically predisposed individuals. Although the precise etiology of IBD remains unclear, accumulating data, including genome-wide association studies, have advanced our understanding of its immunopathogenesis. This review highlights the role in gut homeostasis and IBD pathogenesis of autophagy, the interleukin (IL)-23/IL-17 axis, and a novel member of the tumor necrosis factor family, TL1A. It focuses on advances in our understanding of IBD from the past year, including advances in genetics and immunobiology.