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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. This Article Full Text (PDF) Supplemental Video All Versions of this Article: 2003-07-2209v1 103/6/2397    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Turhan, A. Articles by Frenette, P. S Search for Related Content PubMed PubMed Citation Articles by Turhan, A. Articles by Frenette, P. S Social Bookmarking                   What's this? Submitted July 3, 2003 Accepted October 1, 2003 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* Department of Medicine, Mount Sinai School of Medicine, New York, NY, USA Department of Molecular Genetics and Immunology, Rockefeller University, New York, NY, USA Department of Blood and Vascular Biology, Rockefeller University, New York, NY, USA * Corresponding author; email: paul.frenette{at}mssm.edu. Sickle cell vaso-occlusion is a complex multistep process likely involving heterotypic interactions among sickle erythrocytes (RBCs), leukocytes (WBCs) and endothelial cells. Recent data using intravital microscopy in a sickle cell mouse model suggest that adherent leukocytes in post-capillary 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 non-specific 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 200 mg/kg dramatically reduced these interactions, even after TNF- 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. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: R. Zennadi, A. Chien, K. Xu, M. Batchvarova, and M. J. Telen Sickle red cells induce adhesion of lymphocytes and monocytes to endothelium Blood, October 15, 2008; 112(8): 3474 - 3483. [Abstract] [Full Text] [PDF] N. Mahdi, K. Al-Ola, A. M. Al-Subaie, M. E. Ali, Z. Al-Irhayim, A. Q. Al-Irhayim, and W. Y. Almawi HLA Class II Haplotypes Distinctly Associated with Vaso-Occlusion in Children with Sickle Cell Disease Clin. Vaccine Immunol., April 1, 2008; 15(4): 729 - 731. [Abstract] [Full Text] [PDF] J. Chang, P. A. Shi, E. Y. Chiang, and P. S. Frenette Intravenous immunoglobulins reverse acute vaso-occlusive crises in sickle cell mice through rapid inhibition of neutrophil adhesion Blood, January 15, 2008; 111(2): 915 - 923. [Abstract] [Full Text] [PDF] J. D. Belcher, H. Mahaseth, T. E. Welch, A. E. Vilback, K. M. Sonbol, V. S. Kalambur, P. R. Bowlin, J. C. Bischof, R. P. Hebbel, and G. M. Vercellotti Critical role of endothelial cell activation in hypoxia-induced vasoocclusion in transgenic sickle mice Am J Physiol Heart Circ Physiol, June 1, 2005; 288(6): H2715 - H2725. [Abstract] [Full Text] [PDF] G. R. Buchanan, M. R. DeBaun, C. T. Quinn, and M. H. Steinberg Sickle Cell Disease Hematology, January 1, 2004; 2004(1): 35 - 47. [Abstract] [Full Text] [PDF]

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