Can IL-23 be a good target for ulcerative colitis?

Research output: Contribution to journalReview article

5 Citations (Scopus)

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.

Original languageEnglish
Pages (from-to)95-102
Number of pages8
JournalBest Practice and Research: Clinical Gastroenterology
Volume32-33
DOIs
Publication statusPublished - Feb 1 2018

Fingerprint

Interleukin-23
Ulcerative Colitis
Th17 Cells
Interleukin-12 Subunit p40
Drug and Narcotic Control
Colitis
Intestinal Mucosa
Inflammatory Bowel Diseases
Crohn Disease
Chronic Disease
Therapeutics
Tumor Necrosis Factor-alpha
Monoclonal Antibodies
Cytokines
Inflammation
Safety
Serum
Pharmaceutical Preparations

Keywords

  • Crohn's disease
  • IL-23
  • Inflammatory bowel disease
  • Monoclonal antibody anti-IL23
  • Th17 cell pathway cytokines
  • Ulcerative colitis

ASJC Scopus subject areas

  • Gastroenterology

Cite this

@article{a6dfd46d4e694af7a2ec8bf6ddebe795,
title = "Can IL-23 be a good target for ulcerative colitis?",
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.",
keywords = "Crohn's disease, IL-23, Inflammatory bowel disease, Monoclonal antibody anti-IL23, Th17 cell pathway cytokines, Ulcerative colitis",
author = "Mariangela Allocca and Federica Furfaro and Gionata Fiorino and Daniela Gilardi and Silvia D'Alessio and Silvio Danese",
year = "2018",
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T1 - Can IL-23 be a good target for ulcerative colitis?

AU - Allocca, Mariangela

AU - Furfaro, Federica

AU - Fiorino, Gionata

AU - Gilardi, Daniela

AU - D'Alessio, Silvia

AU - Danese, Silvio

PY - 2018/2/1

Y1 - 2018/2/1

N2 - 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.

AB - 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.

KW - Crohn's disease

KW - IL-23

KW - Inflammatory bowel disease

KW - Monoclonal antibody anti-IL23

KW - Th17 cell pathway cytokines

KW - Ulcerative colitis

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