| Literature DB >> 30060945 |
Mariangela Allocca1, Federica Furfaro2, Gionata Fiorino3, Daniela Gilardi2, Silvia D'Alessio4, Silvio Danese3.
Abstract
A considerable percentage of patients with ulcerative colitis (UC) do not respond to therapies, including anti-tumor necrosis factor (TNF) drugs and vedolizumab, or lose response over time. Hence the continuing need to find new therapeutic strategies and novel drugs to control this chronic debilitating disease. Increased levels of interleukin (IL)-23 and T helper (Th) 17 cell cytokines have been found in intestinal mucosa, plasma, and serum of patients with inflammatory bowel disease (IBD). IL23-blocking has been shown to reduce the severity of inflammation in experimental colitis. Lastly, ustekinumab, a monoclonal antibody (mAb) to the p40 subunit of IL-12 and IL-23, has showed good efficacy and safety profile in patients with Crohn's disease (CD). This review aims to discuss the available data on IL-23 and Th17 cell pathways in UC, in order to define the role of IL-23 as possible target for the treatment of UC.Entities:
Keywords: Crohn's disease; IL-23; Inflammatory bowel disease; Monoclonal antibody anti-IL23; Th17 cell pathway cytokines; Ulcerative colitis
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Year: 2018 PMID： 30060945 DOI： 10.1016/j.bpg.2018.05.016
Source DB: PubMed Journal: Best Pract Res Clin Gastroenterol ISSN： 1521-6918 Impact factor: 3.043