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 Blood, 15 March 2004, Vol. 103, No. 6, pp. 2397-2400.
Prepublished online as a Blood First Edition Paper on November 20, 2003; DOI 10.1182/blood-2003-07-2209.

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RED CELLS
Brief report

Intravenous immune globulin prevents venular vaso-occlusion in sickle cell mice by inhibiting leukocyte adhesion and the interactions between sickle erythrocytes and adherent leukocytes

Aslihan Turhan, Pegah Jenab, Pierre Bruhns, Jeffrey V. Ravetch, Barry S. Coller, and Paul S. Frenette

From the Department of Medicine, Mount Sinai School of Medicine, New York, NY; Laboratory of Blood and Vascular Biology and Laboratory of Molecular Genetics and Immunology, Rockefeller University, New York, NY.

Sickle cell vaso-occlusion is a complex multistep process likely involving heterotypic interactions among sickle erythrocytes (red blood cells [RBCs]), leukocytes (white blood cells [WBCs]), and endothelial cells. Recent data using intravital microscopy in a sickle cell mouse model suggest that adherent leukocytes in postcapillary venules play a critical role in vaso-occlusion by capturing circulating sickle RBCs. In the course of studies to investigate the adhesion receptors mediating sickle RBC-WBC interactions, we found that control nonspecific immunoglobulin G (IgG) preparations displayed significant inhibitory activity. As a result, we studied the effects of commercial intravenous human immune globulin (IVIG) preparations and found that IVIG inhibits RBC-WBC interactions in cremasteric venules in a dose-dependent manner. IVIG of at least 200 mg/kg dramatically reduced these interactions, even after tumor necrosis factor-{alpha} (TNF-{alpha}) stimulation, and not only increased microcirculatory blood flow but also improved survival of sickle cell mice. These data raise the possibility that IVIG may have a beneficial effect on sickle cell–associated vaso-occlusion.


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