Figure 2.

Interactions between microbiota and host genetic and environmental factors contribute to the pathogenesis of IBD. Under healthy conditions (left panel), pathogens are suppressed by beneficial commensal bacteria through the induction of antimicrobial proteins, such as IL-10 and REG3γ, thus maintaining homeostasis. In IBD (right panel), a combination of genetic factors and environmental factors (such as stress, diet, and antibiotic) lead to dysbiosis, which in turn affects barrier integrity, innate, and adaptive immunity, resulting in uncontrolled chronic inflammation and hyper-activation of T helper 1 (Th1) and Th17 cells, increase in tight junction permeability, reduction in regulatory T (Treg) cells, and decrease in REG3γ and IL-10. ATG16L, autophagy-related 16-like; CARD9, caspase recruitment domain family member 9; FUT2, fucosyltransferase 2; IBD, inflammatory bowel disease; IL-10, interleukin 10; IRGM, immunity-related GTPase M; NOD2, nucleotide-binding oligomerization domain-containing protein 2; REG3γ, C-type lectin regenerating islet-derived protein 3γ.