Journal
BLOOD
Volume 109, Issue 1, Pages 219-227Publisher
AMER SOC HEMATOLOGY
DOI: 10.1182/blood-2006-03-007153
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Funding
- NATIONAL CENTER FOR RESEARCH RESOURCES [P20RR015577] Funding Source: NIH RePORTER
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL034363, R37HL034363, P01HL085607] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [T32GM008169] Funding Source: NIH RePORTER
- NCRR NIH HHS [RR15577, P20 RR015577] Funding Source: Medline
- NHLBI NIH HHS [P01 HL085607, HL085607, R01 HL034363, R37 HL034363, HL34363] Funding Source: Medline
- NIGMS NIH HHS [T32 GM008169] Funding Source: Medline
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Cellular turnover is associated with exposure of surface phosphatildylserine (PS) in apoptotic cells, leading to their phagocytic recognition and removal. But recent studies indicate that surface PS exposure is not always associated with apoptosis. Here we show that several members of the human galectin family of glycan binding proteins (galectins-1, -2, and -4) induce PS exposure in a carbohydrate-dependent fashion in activated, but not resting, human neutrophils and in several leukocyte cell lines. PS exposure is not associated with apoptosis in activated neutrophils. The exposure of PS in cell lines treated with these galectins is sustained and does not affect cell viability. Unexpectedly, these galectins bind well to activated T lymphocytes, but do not induce either PS exposure or apoptosis, indicating that galectin's effects are cell specific. These results suggest novel immunoregulatory contribution of galectins in regulating leukocyte turnover independently of apoptosis. (c) 2007 by The American Society of Hematology
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