Galectin-1, an endogenous lectin produced by thymic epithelial cells, induces apoptosis of human thymocytes.
Galectin-1, an endogenous lectin produced by thymic epithelial cells, induces apoptosis of human thymocytes.
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DOI：
10.1084/jem.185.10.1851
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发表时间：
1997-05-19
期刊：
影响因子：
--
通讯作者：
Baum LG
中科院分区：
文献类型：
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作者：
Perillo NL;Uittenbogaart CH;Nguyen JT;Baum LG
Galectin-1 是一种 β-半乳糖苷结合蛋白，由胸腺上皮细胞产生并与人胸腺细胞结合。我们之前报道过galectin-1诱导活化的T淋巴细胞凋亡。由于大多数胸腺细胞仍在胸腺内时通过凋亡而死亡，因此我们测试了 galectin-1 是否可以诱导这些细胞的凋亡。我们现在报道，体外暴露于 galectin-1 诱导了两个 CD4lo CD8lo 胸腺细胞亚群的凋亡。易感胸腺细胞的表型与阴性选择和未选择的细胞一致。胸腺细胞预先暴露于 CD3 抗体可增强 Galectin-1 诱导的细胞凋亡，表明 Galectin-1 可能参与 T 细胞受体介导的细胞凋亡。相反，用地塞米松预处理胸腺细胞对半乳糖凝集素-1的敏感性没有影响。我们注意到，galectin-1 处理后发生凋亡的细胞中有 71% 的 DNA 含量大于 2N，表明增殖的胸腺细胞对 galectin-1 最敏感。我们提出，galectin-1 在负选择和非选择胸腺细胞的凋亡中发挥作用，并且胸腺细胞对 galectin-1 的敏感性部分通过细胞周期的进入或退出来调节。
Galectin-1, a β-galactoside binding protein, is produced by thymic epithelial cells and binds to human thymocytes. We have previously reported that galectin-1 induces the apoptosis of activated T lymphocytes. Because the majority of thymocytes die via apoptosis while still within the thymus, we tested whether galectin-1 could induce the apoptosis of these cells. We now report that in vitro exposure to galectin-1 induced apoptosis of two subsets of CD4lo CD8lo thymocytes. The phenotypes of susceptible thymocytes were consistent with that of both negatively selected and nonselected cells. Galectin-1–induced apoptosis was enhanced by preexposure of thymocytes to antibody to CD3, suggesting that galectin-1 may be a participant in T-cell– receptor mediated apoptosis. In contrast, pretreatment of thymocytes with dexamethasone had no effect on galectin-1 susceptibility. We noted that 71% of the cells undergoing apoptosis after galectin-1 treatment had a DNA content greater than 2N, indicating that proliferating thymocytes were most sensitive to galectin-1. We propose that galectin-1 plays a role in the apoptosis of both negatively selected and nonselected thymocytes, and that the susceptibility of thymocytes to galectin-1 is regulated, in part, by entry or exit from the cell cycle.