Dysregulation of mucosal immune response in pathogenesis of inflammatory bowel disease

World J Gastroenterol. 2014 Mar 28;20(12):3255-64. doi: 10.3748/wjg.v20.i12.3255.

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 17 cells; T helper cells; Ulcerative colitis.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Adaptive Immunity
  • B-Lymphocytes / cytology
  • Colitis, Ulcerative / immunology*
  • Crohn Disease / immunology*
  • Dendritic Cells / cytology
  • Humans
  • Immunity, Innate
  • Immunity, Mucosal / immunology*
  • Inflammation
  • Inflammatory Bowel Diseases / immunology*
  • Interleukin-17 / metabolism
  • Interleukin-23 Subunit p19 / metabolism
  • Interleukins / metabolism
  • Intestinal Mucosa / immunology*
  • Intestinal Mucosa / pathology
  • MicroRNAs / metabolism
  • Th1 Cells / cytology
  • Th2 Cells / cytology

Substances

  • IL23A protein, human
  • IL25 protein, human
  • IL27 protein, human
  • Interleukin-17
  • Interleukin-23 Subunit p19
  • Interleukins
  • MicroRNAs
  • interleukin-21