Galectin-1, an endogenous lectin produced by thymic epithelial cells, induces apoptosis of human thymocytes

被引:255
作者
Perillo, NL
Uittenbogaart, CH
Nguyen, JT
Baum, LG
机构
[1] UNIV CALIF LOS ANGELES, SCH MED, DEPT PATHOL & LAB MED, LOS ANGELES, CA 90095 USA
[2] UNIV CALIF LOS ANGELES, SCH MED, INST MOL BIOL, LOS ANGELES, CA 90095 USA
[3] UNIV CALIF LOS ANGELES, SCH MED, DEPT PEDIAT, LOS ANGELES, CA 90095 USA
[4] UNIV CALIF LOS ANGELES, SCH MED, DEPT MICROBIOL, LOS ANGELES, CA 90095 USA
[5] UNIV CALIF LOS ANGELES, SCH MED, DEPT IMMUNOL, LOS ANGELES, CA 90095 USA
[6] UNIV CALIF LOS ANGELES, SCH MED, JONSSON COMPREHENS CANC CTR, LOS ANGELES, CA 90095 USA
关键词
D O I
10.1084/jem.185.10.1851
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Galectin-1, a beta-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 CD4(lo) CD8(lo) 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.
引用
收藏
页码:1851 / 1858
页数:8
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