Dysregulation of mucosal immune response in pathogenesis of inflammatory bowel disease

Abstract

Inflammatory bowel disease (IBD) includes Crohn’s disease and ulcerative colitis. The exact etiology and pathology of IBD remain unknown. Available evidence suggests that an abnormal immune response against the microorganisms in the intestine is responsible for the disease in genetically susceptible individuals. Dysregulation of immune response in the intestine plays a critical role in the pathogenesis of IBD, involving a wide range of molecules including cytokines. On the other hand, besides T helper (Th) 1 and Th2 cell immune responses, other subsets of T cells, namely Th17 and regulatory T cells, are likely associated with disease progression. Studying the interactions between various constituents of the innate and adaptive immune systems will certainly open new horizons of the knowledge about the immunologic mechanisms in IBD.

Keywords: Crohn’s disease; Inflammatory bowel disease; Proinflammatory cytokines; T helper cells; T helper 17 cells; Ulcerative colitis

Core tip: The etiology and pathology of inflammatory bowel disease (IBD) remain elusive, and dysregulation of the mucosal immune response toward commensal bacterial flora together with genetic and environmental factors may play important roles in the pathogenesis of IBD. A better understanding of the mechanisms of immune responses in the intestinal mucosa will provide new insights into the pathogenesis of IBD, and shed some light on targeted immune therapy for this disease.