The loss of tolerance to CHI3L1 - A putative role in inflammatory bowel disease?
Chitinase-3-like 1 protein
Gastrointestinal tract
Immune response
Inflammation
Inflammatory bowel disease
Journal
Clinical immunology (Orlando, Fla.)
ISSN: 1521-7035
Titre abrégé: Clin Immunol
Pays: United States
ID NLM: 100883537
Informations de publication
Date de publication:
02 2019
02 2019
Historique:
pubmed:
14
12
2018
medline:
4
12
2019
entrez:
14
12
2018
Statut:
ppublish
Résumé
The incidence of inflammatory bowel disease (IBD) is steadily increasing. IBD is characterized by chronic inflammation of the gastrointestinal tract and is divided into the two main entities Crohn's disease (CD) and ulcerative colitis (UC). Genetic predispositions, environmental factors and a dysregulated immune response are known to be involved at the beginning of IBD. However, their etiopathogenesis is not yet fully understood. Over the last ten years, there has been increasing evidence of the involvement of the member of the 18-glycosylhydrolase family chitinase-3-like protein 1 (CHI3L1) in IBD. CHI3L1 is associated with various diseases such as cancer and chronic inflammatory diseases including rheumatoid arthritis or IBD as well as neurological diseases where it can act as a chemoattractant, mitogen or growth factor. This review will focus on the role of autoimmunity to CHI3L1 in IBD in the context of its expression in inflamed colonic epithelia and interaction with intestinal microbiota. Further, it will provide insights into the interaction of CHI3L1 with different mechanisms of the innate and adaptive immune response in IBD.
Identifiants
pubmed: 30543919
pii: S1521-6616(18)30713-7
doi: 10.1016/j.clim.2018.12.005
pii:
doi:
Substances chimiques
CHI3L1 protein, human
0
Chitinase-3-Like Protein 1
0
TLR4 protein, human
0
Toll-Like Receptor 4
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
12-17Informations de copyright
Copyright © 2018. Published by Elsevier Inc.