Dysregulated Tim-3 expression and its correlation with imbalanced CD4 helper T cell function in ulcerative colitis

Dysregulated Tim-3 expression and its correlation with imbalanced CD4 helper T cell function in ulcerative colitis

Copyright © 2012 Elsevier Inc. All rights reserved.

Bibliographische Detailangaben
Veröffentlicht in:Clinical immunology (Orlando, Fla.). - 1999. - 145(2012), 3 vom: 21. Dez., Seite 230-40
1. Verfasser: Shi, Fengmin (VerfasserIn)
Weitere Verfasser: Guo, Xiaoqin, Jiang, Xingwei, Zhou, Ping, Xiao, Yan, Zhou, Tingting, Chen, Guojiang, Zhao, Zhi, Xiao, He, Hou, Chunmei, Li, Xinying, Yang, Xiaomei, Wang, Renxi, Feng, Jiannan, Shen, Beifen, Li, Yan, Han, Gencheng
Format: Online-Aufsatz
Sprache:English
Veröffentlicht: 2012
Zugriff auf das übergeordnete Werk:Clinical immunology (Orlando, Fla.)
Schlagworte:Journal Article Research Support, Non-U.S. Gov't Antibodies, Monoclonal CXCL10 protein, human CXCL9 protein, human Chemokine CXCL10 Chemokine CXCL9 Cxcl10 protein, mouse Cxcl9 protein, mouse Galectins mehr... HAVCR2 protein, human Havcr2 protein, mouse Hepatitis A Virus Cellular Receptor 2 Interleukin-17 LGALS9 protein, human Ligands Membrane Proteins RNA, Messenger Receptors, Virus galectin 9, mouse
Beschreibung
Zusammenfassung:Copyright © 2012 Elsevier Inc. All rights reserved.
The pathogenesis of ulcerative colitis (UC) remains largely unclear. Here we found that T-cell Ig mucin-3 (Tim-3) and its ligand, galectin 9 (Gal-9), were significantly decreased in UC patients and in mice with dextran sodium sulfate (DSS)-induced colitis compared to controls. In addition to an enhanced Th17 response and attenuated regulatory T (Treg) cell response, there was also a significantly decreased Th1 response in UC. Levels of the Th1 cell chemokines CXCL9 and CXCL10 were significantly decreased in UC mice, partially explaining the decreased Th1 cell function in UC. Finally, administration of a putative antagonistic anti-Tim-3 antibody or of recombinant Gal-9 significantly exacerbated or attenuated DSS-induced colitis by altering the balance between different Th cell subsets. Our data suggest that a dysregulated Tim-3/Gal-9 pathway may contribute to the pathogenesis of UC. A better understanding of this pathway may shed new light on the pathogenesis of this disease
Beschreibung:Date Completed 17.01.2013
Date Revised 25.11.2016
published: Print-Electronic
Citation Status MEDLINE
ISSN:1521-7035
DOI:10.1016/j.clim.2012.09.001