Immunopathogenesis of inflammatory bowel disease

World J Gastroenterol. 2008 Jan 21;14(3):390-400. doi: 10.3748/wjg.14.390.

Abstract

Crohn's disease and ulcerative colitis are chronic relapsing immune mediated disorders that results from an aberrant response to gut luminal antigen in genetically susceptible host. The adaptive immune response that is then triggered was widely considered to be a T-helper-1 mediated condition in Crohn's disease and T-helper-2 mediated condition in ulcerative colitis. Recent studies in animal models, genome wide association, and basic science has provided important insights in in the immunopathogenesis of inflammatory bowel disease, one of which was the characterization of the interleukin-23/Th-17 axis.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • CARD Signaling Adaptor Proteins / genetics
  • CARD Signaling Adaptor Proteins / metabolism
  • Epithelial Cells / cytology
  • Epithelial Cells / metabolism
  • Humans
  • Immunity, Innate / physiology
  • Inflammatory Bowel Diseases* / etiology
  • Inflammatory Bowel Diseases* / immunology
  • Inflammatory Bowel Diseases* / pathology
  • Interleukin-17 / immunology
  • Interleukin-23 / immunology
  • Intestinal Mucosa / cytology
  • Intestinal Mucosa / microbiology
  • Intestinal Mucosa / pathology
  • T-Lymphocytes / immunology
  • Toll-Like Receptors / genetics
  • Toll-Like Receptors / metabolism

Substances

  • CARD Signaling Adaptor Proteins
  • Interleukin-17
  • Interleukin-23
  • Toll-Like Receptors