No conflicts of interest were declared.
Innate immunity in inflammatory bowel disease: a disease hypothesis†
Version of Record online: 27 DEC 2007
Copyright © 2007 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
The Journal of Pathology
Special Issue: Molecular and cellular themes in inflammation and immunology
Volume 214, Issue 2, pages 260–266, January 2008
How to Cite
Marks, D. and Segal, A. (2008), Innate immunity in inflammatory bowel disease: a disease hypothesis. J. Pathol., 214: 260–266. doi: 10.1002/path.2291
- Issue online: 27 DEC 2007
- Version of Record online: 27 DEC 2007
- Wellcome Trust
Crohn's disease arises from a defective interaction between the highly concentrated mass of bacteria in the gastrointestinal tract and the underlying tissues. It has generally been believed to result from an excessively exuberant inflammatory response or from ‘autoimmunity’. Recent evidence has emerged that the problem is instead a failure of the way in which the body responds to the penetration of bacteria and other bowel contents through the intestinal mucosal barrier. Rather than Crohn's disease being caused by excessive inflammation, the primary mechanism is actually that of an immunodeficiency. Failure of inflammatory mediator production leads to insufficient recruitment of neutrophils, resulting in inadequate removal of bacteria and other debris. This impairment of acute inflammation can be compensated in some circumstances by signalling through NOD2. If not cleared, the foreign material in the bowel wall is taken up within macrophages, eliciting a granulomatous reaction and the local and systemic sequelae so characteristic of Crohn's disease. Copyright © 2007 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.