Author/Authors :
Shi، نويسنده , , Fengmin and Guo، نويسنده , , Xiaoqin and Jiang، نويسنده , , Xingwei and Zhou، نويسنده , , Ping and Xiao، نويسنده , , Yan and Zhou، نويسنده , , Tingting and Chen، نويسنده , , Guojiang and Zhao، نويسنده , , Zhi and Xiao، نويسنده , , He and Hou، نويسنده , , ChunMei and Li، نويسنده , , Xinying and Yang، نويسنده , , Xiaomei and Wang، نويسنده , , Renxi and Feng، نويسنده , , Jiannan and Shen، نويسنده , , Beifen and Li، نويسنده , , Ya، نويسنده ,
Abstract :
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.
Keywords :
TIM-3 , Gal-9 , T help cells , ulcerative colitis , Immune regulation
