Interleukin‐23/Th17 pathways and inflammatory bowel disease

• Published in: Inflammatory bowel diseases 2009-07, Vol.15 (7), p.1090-1100
• Main Authors: Abraham, Clara, Cho, Judy
• Format: Article
• Language: English
• Subjects: Animals; autoimmunity; CD4-Positive T-Lymphocytes - immunology; CD4-Positive T-Lymphocytes - metabolism; Humans; IL‐23; inflammation; inflammatory bowel disease; Inflammatory Bowel Diseases - immunology; Inflammatory Bowel Diseases - metabolism; Interleukin-17 - immunology; Interleukin-17 - metabolism; Interleukin-23 - immunology; Interleukin-23 - metabolism; Signal Transduction - immunology; Th17 cells
• ISSN: 1078-0998; 1536-4844
• DOI: 10.1002/ibd.20894

The IL‐23/Th17 pathway has recently been identified to play a critical role in a number of chronic inflammatory diseases including inflammatory bowel disease (IBD). The identification in IBD patients of associations in IL23R and regions that include other genes in the IL‐23/Th17 pathway has highlighted the importance of proper IL‐23/Th17 pathway regulation in intestinal immune homeostasis. IL‐23 plays a role in CD4+ Th17 lineage cells, characterized by IL‐17 secretion and the expression of the transcription factor retinoic acid‐related orphan receptor (ROR)γτ, and in other immune and nonimmune cells. The balance between effector T cell subsets, such as Th17 cells, and CD4+ T regulatory subsets is finely regulated; dysregulation of this balance can lead to inflammation and autoimmunity. As such, the IL‐23/Th17 pathway contributes to immune responses that play a role in defenses to microbial infection, as well as in the intestinal inflammation observed in both animal models of colitis and human IBD. (Inflamm Bowel Dis 2009)