©The Author(s) 2017. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Jun 14, 2017; 23(22): 3964-3977
Published online Jun 14, 2017. doi: 10.3748/wjg.v23.i22.3964
Published online Jun 14, 2017. doi: 10.3748/wjg.v23.i22.3964
Molecular mimicry in Helicobacter pylori infections
Magdalena Chmiela, Weronika Gonciarz, Department of Immunology and Infectious Biology, Institute of Microbiology, Biotechnology and Immunology, Faculty of Biology and Environmental Protection, University of Lodz, 90-237 Lodz, Poland
Author contributions: Chmiela M designed and wrote the manuscript; Gonciarz W wrote some parts of the manuscript and designed the figure.
Supported by the National Science Center grants , No. UMO-2013/09/N/NZ6/00805 and No. UMO-2015/17/N/NZ6/03490 .
Conflict-of-interest statement: No potential conflict of interest.
Correspondence to: Magdalena Chmiela, MD, PhD, Professor, Department of Immunology and Infectious Biology, Institute of Microbiology, Biotechnology and Immunology, Faculty of Biology and Environmental Protection, University of Lodz, Banacha 12/16, 90-237 Lodz, Poland. chmiela@biol.uni.lodz.pl
Telephone: +48-42-6354186 Fax: +48-42-6655818
Received: January 18, 2017
Peer-review started: January 21, 2017
First decision: February 9, 2017
Revised: May 16, 2017
Accepted: June 1, 2017
Article in press: June 1, 2017
Published online: June 14, 2017
Processing time: 146 Days and 9.8 Hours
Peer-review started: January 21, 2017
First decision: February 9, 2017
Revised: May 16, 2017
Accepted: June 1, 2017
Article in press: June 1, 2017
Published online: June 14, 2017
Processing time: 146 Days and 9.8 Hours
Core Tip
Core tip: Molecular mimicry between Helicobacter pylori (H. pylori) and the host structures has been suggested as an effective mechanism of antibody production, potentially autoreactive. The chronic character of H. pylori infections increases the risk of such production and initiation or maintenance of H. pylori related pathological disorders triggered by the host effector immune mechanisms during infection. The panel of components common to H. pylori and the host is still increasing and thus the risk of autoimmune complications is an open problem.