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The Journal of Immunology, 2002, 169: 5912-5918.
Copyright © 2002 by The American Association of Immunologists

Selective Eosinophil Adhesion to Fibroblast Via IFN-{gamma}-Induced Galectin-9

Hirofumi Asakura*, Yumiko Kashio{dagger}, Kazuhiro Nakamura{dagger}, Masako Seki{dagger}, Shuyan Dai{ddagger}, Yukako Shirato{dagger}, Mohammad J. Abedin{dagger}, Naoko Yoshida{dagger}, Nozomu Nishi§, Tadaatsu Imaizumi, Naoki Saita||, Yoshihiro Toyama*, Hitoshi Takashima*, Takanori Nakamura§, Motoomi Ohkawa* and Mitsuomi Hirashima1,{dagger}

Departments of * Radiology, {dagger} Immunology and Immunopathology, {ddagger} Perinatology and Gynecology, and § Endocrinology, Kagawa Medical University, Kagawa, Japan; Department of Vascular Biology, Institute of Brain Science, Hirosaki University School of Medicine, Hirosaki, Japan; and || First Department of Internal Medicine, Kumamoto University School of Medicine, Kumamoto, Japan

Among galectin family members, galectin-9 was first described as a potent eosinophil chemoattractant derived from Ag-stimulated T cells. In the present study a role of galectin-9 in the interaction between eosinophils and fibroblasts was investigated using a human lung fibroblast cell line, HFL-1. RT-PCR, real-time PCR, and Western blot analyses revealed that both galectin-9 mRNA and protein in HFL-1 cells were up-regulated by IFN-{gamma} stimulation. On the one hand, IL-4, known as a Th2 cytokine, did not affect the galectin-9 expression in HFL-1 cells. We further confirmed that IFN-{gamma} up-regulated the expression of galectin-9 in primary human dermal fibroblasts. Flow cytometric analysis revealed that IFN-{gamma} up-regulated surface galectin-9 expression on HFL-1 cells. Stimulation of HFL-1 cells with IFN-{gamma} up-regulated adhesion of eosinophils, but not neutrophils, to HFL-1 cells. This adherence of eosinophils to HFL-1 cells was inhibited by both lactose and anti-galectin-9 Ab. These findings demonstrate that IFN-{gamma}-induced galectin-9 expression in fibroblasts mediates eosinophil adhesion to the cells, suggesting a crucial role of galectin-9 in IFN-{gamma}-stimulated fibroblasts as a physiological modulator at the inflammatory sites.




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