Immunopathogenesis of IBD: current concepts.

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Immunopathogenesis of inflammatory bowel disease: current

concepts.

Inflammatory

bowel disease

Current

Opinion in Gastroenterology. July 2007.

Bamias, Giorgos a; Cominelli, Fabio b

Abstract:

Purpose of review: According to the current paradigm, ulcerative colitis and

Crohn's disease occur in genetically predisposed individuals because of dysregulated immune responses against intraluminal

bacterial antigens. Data have recently accumulated

supporting alternative hypotheses for the pathogenesis of inflammatory bowel

disease. Here, we present novel immunogenetic

pathways and discuss their impact on traditional understanding of inflammatory

bowel disease.

Recent findings: In the

gastrointestinal tract the innate immune system contains intraluminal

bacteria locally, avoiding invasion of the deeper layers and preventing

induction of long-standing proinflammatory responses. Failure of this protective function of the innate immune

system appears to be the primary defect in inflammatory bowel disease, as a

result of impairment of NOD2 signaling or other unidentified deficiencies. The adaptive immune response that ensues was thought to be

strictly differentiated between T-helper-1 mediated in Crohn's disease and

T-helper-2 mediated in ulcerative colitis. This

concept is rapidly changing, however, in light of recent evidence suggesting

that tissue injury in inflammatory bowel disease is mediated by novel effector pathways, the most prominent of which is the interleukin-23/Th17

axis.

Summary: Elucidation of the

pathways that underlie chronic intestinal inflammation will facilitate the

development of new treatments with increased specificity and probably with

decreased toxicity.

© 2007 Lippincott

& Wilkins, Inc.

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