Galectin-1: a key effector of regulation mediated by CD4+CD25+ T cells.

Journal article

The naturally occurring population of dedicated regulatory T cells that coexpress CD4 and CD25 is known to play a key role in the maintenance of peripheral T-cell tolerance; however, their mechanism of action has remained obscure. Here we report that a member of the family of beta-galactoside-binding proteins, galectin-1, is overexpressed in regulatory T cells, and that expression is increased after activation. Most importantly, blockade of galectin-1 binding significantly reduced the inhibitory effects of human and mouse CD4+CD25+ T cells. Reduced regulatory activity was observed in CD4+CD25+ T cells obtained from galectin-1-homozygous null mutant mice. These results suggest that galectin-1 is a key effector of the regulation mediated by these cells.

Authors: Garín, M; Chu, C; Golshayan, D; Cernuda-Morollón, E; Wait, R

• Publication status: Published
• Journal: Blood
• Volume: 109
• Issue: 5
• Pages: 2058-2065
• Publication date: 2007-03-01
• DOI: 10.1182/blood-2006-04-016451
• EISSN: 1528-0020
• ISSN: 0006-4971
• Language: English
• Keywords: Cytoplasm; Cell Separation; Interleukin-2 Receptor alpha Subunit; Immunoprecipitation; Receptors, Antigen, T-Cell; Biological Markers; Animals; Galectin 1; T-Lymphocytes, Regulatory; Lymphocyte Activation; Humans; Mice; CD4-Positive T-Lymphocytes; Cells, Cultured; Antibodies, Monoclonal; Cell Nucleus; Culture Media