Open AccessInterleukin‐23/Th17 pathways and inflammatory bowel disease
Author(s) -
Abraham Clara,
Cho Judy
Publication year - 2009
Publication title -
inflammatory bowel diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.932
H-Index - 146
eISSN - 1536-4844
pISSN - 1078-0998
DOI - 10.1002/ibd.20894
Subject(s) - rar related orphan receptor gamma , interleukin 23 , inflammatory bowel disease , immunology , inflammation , immune system , orphan receptor , autoimmunity , interleukin 17 , biology , regulatory t cell , t cell , medicine , transcription factor , disease , foxp3 , il 2 receptor , gene , genetics
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)