Journal
BLOOD
Volume 109, Issue 5, Pages 2058-2065Publisher
AMER SOC HEMATOLOGY
DOI: 10.1182/blood-2006-04-016451
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Funding
- Medical Research Council [G9900166] Funding Source: Medline
- Medical Research Council [G9900166] Funding Source: researchfish
- MRC [G9900166] Funding Source: UKRI
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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 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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