单位：[1]Department of Clinical Laboratory, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China华中科技大学同济医学院附属同济医院检验科[2]Department of Neurology, Beijing Tiantan Hospital, Capital Medical University, Beijing 100050, China首都医科大学附属天坛医院[3]Institute of Organ Transplantation, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China华中科技大学同济医学院附属同济医院器官移植研究所器官移植
T cell immunoglobulin and mucin domain (Tim)-3 is expressed on activated CD4(+) and CD8(+) T cells. Identification of galectin-9 as a ligand for Tim-3 has now firmly established the Tim-3/galectin-9 pathway, which results in apoptosis of effector CD4(+). and CD8(+) T cells. Moreover, Th17 cells are a recently discovered CD4(+) effector T cell, which are important in antimicrobial immunity. Whether the Tim-3/galectin-9 pathway affects Th17 immunity has not been elucidated. Here, we demonstrated expression of Tim-3 on Th17 cells by flow cytometry. Th17-skewed cells were sensitive to galectin-9-induced apoptosis. In vitro administration of galectin-9 decreased stimulated Th17 cells and inhibited production of IL-17. Interestingly, Klebsiella pneumoniae (K. pneumoniae) infection led to enhanced IL-17 levels. Recombinant galectin-9 significantly decreased IL-17 in vivo, which resulted in reduced bacterial clearance and high mortality. These observations suggest that the Tim-3/galectin-9 pathway plays an important role in termination of Th17-immune responses, and could be a therapeutic target for inflammatory diseases. (C) 2011 Elsevier Inc. All rights reserved.
第一作者单位：[1]Department of Clinical Laboratory, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China
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wang feng,xu jie,liao yalong,et al.Tim-3 ligand galectin-9 reduces IL-17 level and accelerates Klebsiella pneumoniae infection[J].CELLULAR IMMUNOLOGY.2011,269(1):22-28.doi:10.1016/j.cellimm.2011.03.005.
