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Galectin-1: a key effector of regulation mediated by CD4+CD25+ T cells
Authors:Garín Marina I  Chu Chung-Ching  Golshayan Dela  Cernuda-Morollón Eva  Wait Robin  Lechler Robert I
Affiliation:Immunoregulation Laboratory, Department of Nephrology and Transplantation, King's College London School of Medicine at Guy's, King's College and St Thomas' Hospitals, London, United Kingdom.
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 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.
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