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

447Citations
Citations of this article
265Readers
Mendeley users who have this article in their library.

This article is free to access.

Abstract

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 β-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+ Tcells 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. © 2007 by The American Society of Hematology.

Cite

CITATION STYLE

APA

Garín, M. I., Chu, N. C., Golshayan, D., Cernuda-Morollón, E., Wait, R., & Lechler, R. I. (2007). Galectin-1: A key effector of regulation mediated by CD4 +CD25+ T cells. Blood, 109(5), 2058–2065. https://doi.org/10.1182/blood-2006-04-016451

Register to see more suggestions

Mendeley helps you to discover research relevant for your work.

Already have an account?

Save time finding and organizing research with Mendeley

Sign up for free