학술논문

Galectin-1, an endogenous lectin produced by thymic epithelial cells, induces apoptosis of human thymocytes.
Document Type
article
Source
The Journal of experimental medicine. 185(10)
Subject
Epithelium
Thymus Gland
T-Lymphocyte Subsets
T-Lymphocytes
CD4-Positive T-Lymphocytes
CD8-Positive T-Lymphocytes
Cells
Cultured
Humans
Dithiothreitol
Lectins
Galectin 1
Recombinant Proteins
DNA
Hemagglutinins
Flow Cytometry
Apoptosis
Models
Immunological
Cells
Cultured
Models
Immunological
Medical and Health Sciences
Immunology
Language
Abstract
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.