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Published on: April 21, 2015
Dysregulated Tim-3 expression and its correlation with imbalanced CD4 helper T cell function in ulcerative colitis.
Fengmin Shi1, Xiaoqin Guo, Xingwei Jiang
1Department of Molecular Immunology, Institute of Basic Medical Sciences, Beijing 100850, China.
Clinical Immunology (Orlando, Fla.)
|November 3, 2012
Summary
The T-cell Ig mucin-3 (Tim-3) and galectin 9 (Gal-9) pathway is altered in ulcerative colitis (UC). Dysregulation of this pathway may contribute to UC pathogenesis, offering new therapeutic targets.
Area of Science:
- Immunology
- Gastroenterology
Background:
- The exact causes of ulcerative colitis (UC) are not fully understood.
- Immune dysregulation plays a key role in UC pathogenesis.
Purpose of the Study:
- To investigate the role of the T-cell Ig mucin-3 (Tim-3) and galectin 9 (Gal-9) pathway in UC.
- To explore the impact of Tim-3/Gal-9 dysregulation on T helper cell responses in UC.
Main Methods:
- Compared Tim-3 and Gal-9 levels in UC patients and DSS-induced colitis mice versus controls.
- Analyzed Th17, Treg, and Th1 cell responses and associated chemokines (CXCL9, CXCL10).
- Administered anti-Tim-3 antibody or recombinant Gal-9 in DSS-induced colitis models.
Main Results:
- Tim-3 and Gal-9 were significantly decreased in UC patients and models.
- UC exhibited enhanced Th17, reduced Treg, and decreased Th1 responses, with lower CXCL9/CXCL10 levels.
- Anti-Tim-3 exacerbated colitis, while Gal-9 attenuated it by modulating T helper cell balance.
Conclusions:
- A dysregulated Tim-3/Gal-9 pathway is implicated in UC pathogenesis.
- Targeting the Tim-3/Gal-9 pathway may offer novel therapeutic strategies for UC.
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