The IL-23/IL-17 pathway in inflammatory bowel disease.

Abstract

The etiology of inflammatory bowel disease is unknown but available evidence suggests that a deregulated immune response towards the commensal bacterial flora is responsible for intestinal inflammation in genetically predisposed individuals. IL-23 promotes expansion and maintenance of Th17 cells, which secrete the proinflammatory cytokine IL-17 and have been implicated in the pathogenesis of many chronic inflammatory disorders. Recent studies have shown that IL-23 also acts on cells of the innate immune system that can contribute to inflammatory cytokine production and tissue inflammation. A role for the IL-23/IL-17 pathway in the pathogenesis of chronic intestinal inflammation in inflammatory bowel disease has emerged from both animal and human studies. Here we aim to review the recent advances in this rapidly moving field.

• Authors: Alessandra Geremia, Derek P Jewell
• Journal: Expert review of gastroenterology & hepatology (Expert Rev Gastroenterol Hepatol) Vol. 6 Issue 2 Pg. 223-37 (Apr 2012) ISSN: 1747-4132 [Electronic] England
• PMID: 22375527 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Review)

Chemical References

• Inflammation Mediators
• Interleukin-17
• Interleukin-23

Topics

• Animals
• Colitis, Ulcerative (genetics, immunology, microbiology)
• Crohn Disease (genetics, immunology, microbiology)
• Humans
• Immunity, Innate
• Inflammation Mediators (metabolism)
• Interleukin-17 (metabolism)
• Interleukin-23 (metabolism)
• Intestines (immunology, microbiology)
• Signal Transduction
• Th17 Cells (immunology)