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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.


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IMMUNOBIOLOGY

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

Marina I. Garín1,5, Chung-Ching Chu1, Dela Golshayan1,2, Eva Cernuda-Morollón3, Robin Wait4, and Robert I. Lechler1

1 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; 2 Division of Nephrology and Transplant Centre, Centre Hospitalier Universitaire Vaudois (CHUV), Lausanne, Switzerland; 3 Ludwig Institute for Cancer Research, Royal Free and University College School of Medicine, London, United Kingdom; 4 Kennedy Institute of Rheumatology, Arthritis Research Campaign Building, Faculty of Medicine, Imperial College London, United Kingdom; 5 Laboratorio de Hematopoyesis y Terapia Génica, Centro de Investigaciones Energéticas Medioambientales y Tecnológicas (CIEMAT), Madrid, Spain

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 ß-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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