IBD and Th17 cells (contd.)

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Curr Opin Gastroenterol. 2007 Jul;23(4):365-9.

Immunopathogenesis of inflammatory bowel disease: current concepts.

Bamias G, Cominelli F.

aFirst Department of Propaedeutic Medicine, Laiko General Hospital,

Athens, Greece bDigestive Health Center of Excellence, University of

Virginia Health System, Charlottesville, Virginia, USA.

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. PMID: 17545770.