Editorial
Copyright ©The Author(s) 2018. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastrointest Pathophysiol. Nov 12, 2018; 9(4): 73-78
Published online Nov 12, 2018. doi: 10.4291/wjgp.v9.i4.73
Role of TNFSF15 in the intestinal inflammatory response
Tanya Kadiyska, Ivan Tourtourikov, Ana-Maria Popmihaylova, Hilda Kadian, Ani Chavoushian
Tanya Kadiyska, Department of Medical Chemistry and Biochemistry, Sofia Medical University, Sofia 1431, Bulgaria
Tanya Kadiyska, Ivan Tourtourikov, Genetic Medico-Diagnostic Laboratory Genica, Sofia 1612, Bulgaria
Ana-Maria Popmihaylova, University of Montpellier, Montpellier 34090, France
Hilda Kadian, Bulgarian Association for Inflammatory Bowel Diseases, Sofia 1527, Bulgaria
Ani Chavoushian, Department of Gastroenterology, Acibadem City Clinic Oncology Center, Sofia 1784, Bulgaria
Author contributions: All authors contributed equally to the research for this manuscript; Tourtourikov I and Kadiyska T approved the final version of the article.
Conflict-of-interest statement: The authors have no conflict of interest to declare.
Open-Access: This is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: Tanya Kadiyska, PhD, Assistant Professor, Department of Medical Chemistry and Biochemistry, Sofia Medical University, 2 Zdrave str., Sofia 1431, Bulgaria. kadiyska_t@yahoo.com
Telephone: +359-2-9530715 Fax: +359-2-9530715
Received: August 3, 2018
Peer-review started: August 3, 2018
First decision: August 30, 2018
Revised: October 11, 2018
Accepted: October 17, 2018
Article in press: October 18, 2018
Published online: November 12, 2018
Processing time: 101 Days and 10.9 Hours
Abstract

Gastrointestinal diseases, specifically Crohn’s disease, ulcerative colitis, diverticular disease, and primary biliary cirrhosis are all characterized by complicated inflammation of the digestive tract. Their pathology is multifactorial, and risk factors encompass both genetic and environmental factors. Recent advances in the genetic component of inflammatory bowel diseases (IBDs) have revealed that the tumor necrosis factor superfamily member 15 (TNFSF15) contains a number of risk alleles associated not only with IBD but also with other diseases such as diverticular disease and primary biliary cirrhosis. These risk alleles in TNFSF15 and the altered expression of its gene product can serve as the common ground between these disorders by explaining at least some of the underlying processes that lead to a dysregulated immune response and subsequent chronic inflammation. Here, we aim to outline how the TNFSF15 gene is involved in the proliferation and cell fate of different populations of T cells and subsequently in the control of both pro- and anti-inflammatory cytokines. Furthermore, we summarize what is currently known of TNFSF15 control region variants, how they are associated with each mentioned disease, and how these variants can explain the autoimmune pathology of said diseases through altered TNFSF15 expression.

Keywords: Tumor necrosis factor superfamily member 15; Diverticular disease; Death receptor 3; Ulcerative colitis; Crohn’s disease; Primary biliary cirrhosis

Core tip: Tumor necrosis factor superfamily member 15 and the protein it encodes, tumor necrosis factor ligand-related molecule 1 play a vital role in the mucosal immunity. Expression of tumor necrosis factor ligand-related molecule 1 and death receptor 3-mediated signaling both exert their effects in Crohn’s disease, ulcerative colitis, diverticular disease, and primary biliary cirrhosis, which can serve to bridge the gap of knowledge regarding the genetic components of this group of inflammatory diseases as well as provide common ground for a putative targeted treatment.