The pathogenesis of mucosal inflammation in murine models of inflammatory bowel disease and Crohn disease

Ann Intern Med. 1998 May 15;128(10):848-56. doi: 10.7326/0003-4819-128-10-199805150-00009.


In recent years, it has become apparent that overproduction of the Th1 cytokines interleukin-12 and interferon-gamma is the probable driving force behind murine models of intestinal inflammation resembling Crohn disease and intestinal inflammation in humans with Crohn disease. In addition, studies of murine models strongly suggest that this overproduction is associated with inadequate secretion of the counter-regulatory and anti-inflammatory cytokine transforming growth factor-beta. Thus, mucosal inflammation in models (and possibly in humans) may result from an imbalance between normally occurring positive (immunogenic or inflammatory) responses and negative (tolerogenic or anti-inflammatory) mucosal immune responses. These new findings and the hypotheses that arise from them are being used to construct new approaches to the treatment of Crohn disease that are based on the administration of anti-inflammatory cytokines and anti-cytokine antibodies.

Publication types

  • Consensus Development Conference
  • Review

MeSH terms

  • Animals
  • Antibodies / therapeutic use
  • Crohn Disease / immunology*
  • Crohn Disease / pathology
  • Crohn Disease / therapy
  • Cytokines / biosynthesis
  • Cytokines / immunology
  • Cytokines / therapeutic use
  • Disease Models, Animal
  • Inflammatory Bowel Diseases / immunology*
  • Inflammatory Bowel Diseases / pathology
  • Inflammatory Bowel Diseases / therapy
  • Intestinal Mucosa / immunology*
  • Intestinal Mucosa / pathology
  • Mice
  • Mice, Knockout


  • Antibodies
  • Cytokines