Inflammatory bowel disease: cause and immunobiology

Lancet. 2007 May 12;369(9573):1627-40. doi: 10.1016/S0140-6736(07)60750-8.


Crohn's disease and ulcerative colitis are idiopathic inflammatory bowel disorders. In this paper, we discuss how environmental factors (eg, geography, cigarette smoking, sanitation and hygiene), infectious microbes, ethnic origin, genetic susceptibility, and a dysregulated immune system can result in mucosal inflammation. After describing the symbiotic interaction of the commensal microbiota with the host, oral tolerance, epithelial barrier function, antigen recognition, and immunoregulation by the innate and adaptive immune system, we examine the initiating and perpetuating events of mucosal inflammation. We pay special attention to pattern-recognition receptors, such as toll-like receptors and nucleotide-binding-oligomerisation-domains (NOD), NOD-like receptors and their mutual interaction on epithelial cells and antigen-presenting cells. We also discuss the important role of dendritic cells in directing tolerance and immunity by modulation of subpopulations of effector T cells, regulatory T cells, Th17 cells, natural killer T cells, natural killer cells, and monocyte-macrophages in mucosal inflammation. Implications for novel therapies, which are discussed in detail in the second paper in this Series, are covered briefly.

Publication types

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

MeSH terms

  • Environmental Exposure / adverse effects*
  • Genetic Predisposition to Disease*
  • Humans
  • Immune System / physiology*
  • Inflammatory Bowel Diseases* / etiology
  • Inflammatory Bowel Diseases* / genetics
  • Inflammatory Bowel Diseases* / immunology
  • Intestines / immunology
  • Karyotyping
  • Life Style
  • Nod Signaling Adaptor Proteins / immunology
  • Nod Signaling Adaptor Proteins / physiology*
  • Prevalence
  • Risk Factors


  • Nod Signaling Adaptor Proteins