STAT3-activating cytokines: a therapeutic opportunity for inflammatory bowel disease?
- Author(s)
- Nguyen, PM; Putoczki, TL; Ernst, M;
- Details
- Publication Year 2015-03-11,Volume 35,Issue #5,Page 340-50
- Journal Title
- J Interferon Cytokine Res
- Publication Type
- Journal Article
- Abstract
- The gastrointestinal tract is lined by a single layer of epithelial cells that secrete mucus toward the lumen, which collectively separates the immune sentinels in the underlying lamina propria from the intestinal microflora to prevent aberrant immune responses. Inflammatory bowel disease (IBD) describes a group of autoimmune diseases that arise from defects in epithelial barrier function and, as a consequence, aberrant production of inflammatory cytokines. Among these, interleukin (IL)-6, IL-11, and IL-22 are elevated in human IBD patients and corresponding mouse models and, through activation of the JAK/STAT3 pathway, can both propagate and ameliorate disease. In particular, cytokine-mediated activation of STAT3 in the epithelial lining cells affords cellular protection, survival, and proliferation, thereby affording therapeutic opportunities for the prevention and treatment of colitis. In this review, we focus on recent insights gained from therapeutic modulation of the activities of IL-6, IL-11, and IL-22 in models of IBD and advocate a cautionary approach with these cytokines to minimize their tumor-promoting activities on neoplastic epithelium.
- Publisher
- Liebert
- Research Division(s)
- Inflammation
- PubMed ID
- 25760898
- Publisher's Version
- https://doi.org/10.1089/jir.2014.0225
- Open Access at Publisher's Site
http://online.liebertpub.com/doi/10.1089/jir.2014.0225- NHMRC Grants
- NHMRC/1008614, NHMRC/1080498, NHMRC/603122, NHMRC/1069024,
- Terms of Use/Rights Notice
- Refer to copyright notice on published article.
Creation Date: 2015-05-21 08:48:37
Last Modified: 2015-05-21 08:58:58