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Blood, 1 January 2007, Vol. 109, No. 1, pp. 219-227.
Prepublished online as a Blood First Edition Paper on August 29, 2006; DOI 10.1182/blood-2006-03-007153.


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Submitted March 7, 2006
Accepted August 9, 2006

Human Galectins-1, -2, and -4 induce surface exposure of phosphatidylserine in activated human neutrophils but not activated T cells

Sean Stowell, Sougata Karmakar, Caleb Stowell, Marcelo Dias-Baruffi, Rodger P McEver, and Richard D Cummings*

Biochemistry & Molecular Biology, University of Oklahoma Health Sciences Center, Oklahoma City, OK
Cardiovascular Biology Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK,USA

* Corresponding author; email: rdcummi{at}emory.edu.

Cellular turnover is associated with exposure of surface phosphatidylserine (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 effects are cell specific. These results suggest novel immunoregulatory contribution of galectins in regulating leukocyte turnover independently of apoptosis.


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