Editorial
Copyright ©2007 Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Nov 14, 2007; 13(42): 5547-5551
Published online Nov 14, 2007. doi: 10.3748/wjg.v13.i42.5547
Emerging role of IL-23/IL-17 axis in H pylori-associated pathology
Roberta Caruso, Francesco Pallone, Giovanni Monteleone
Roberta Caruso, Francesco Pallone, Giovanni Monteleone, Department of Internal Medicine & Centre of Excellence for Genomic Risk Assessment in Multifactorial and Complex Diseases, University "Tor Vergata" of Rome, Rome, Italy
Author contributions: All authors contributed equally to the work.
Correspondence to: Giovanni Monteleone, Cattedra di Gastroenterologia, Dipartimento di Medicina Interna, Università Tor Vergata, Via Montpellier, 1, Rome 00133, Italy. gi.monteleone@med.uniroma2.it
Telephone: +39-6-72596158 Fax: +39-6-72596391
Received: July 3, 2007
Revised: August 10, 2007
Accepted: September 9, 2007
Published online: November 14, 2007
Abstract

Colonization of stomach by H pylori is followed by a marked infiltration of the mucosa with polymorphonuclear leukocytes, macrophages, and lymphocytes that very often remains asymptomatic, but in some circumstances can lead to the development of gastroduodenal ulceration, gastric carcinoma, and mucosa-associated lymphoid tissue lymphoma. The molecular mechanisms by which H pylori triggers and maintains the local immune response are complex, but there is evidence that cytokines produced by both immune and non-immune cells contribute to amplify the ongoing inflammation. H pylori infection is associated with a marked mucosal induction of T helper (Th) type 1 and Th17-type cytokines that is governed by specific antigen-presenting cell-derived molecules, such as interleukin (IL)-12 and IL-23. In this paper, we will review the available data on the expression and role of IL-23 and IL-17 in H pylori-related gastritis.

Keywords: IL-23, IL-17, H pylori