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Blood, 1 March 2007, Vol. 109, No. 5, pp. 2058-2065.
Prepublished online as a Blood First Edition Paper on November 16, 2006; DOI 10.1182/blood-2006-04-016451.
Previous Article | Next Article 
Submitted April 17, 2006
Accepted September 26, 2006
Galectin-1: a key effector of regulation mediated by
CD4+CD25+ T cells
Marina I Garin, Chung-Ching Chu, Dela Golshayan, Eva Cernuda-Morollon, Robin Wait, and Robert I Lechler*
Laboratorio de Hematopoyesis y Terapia Genica, CIEMAT, Madrid, Spain
Department of Nephrology and Transplantation, King's College and St. Thomas' Hospitals, London, United Kingdom
Division of Nephrology and Transplant Centre, CHUV, Lausanne, Switzerland
Ludwig Institute for Cancer Research, Royal Free and University College School of Medicine, London, United Kingdom
Kennedy Institute of Rheumatology, Imperial College London, London, United Kingdom
* Corresponding author; email: robert.lechler{at}kcl.ac.uk.
The naturally occurring population of dedicated regulatory T cells that co-express 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 -galactoside-binding proteins, galectin-1, is over-expressed 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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