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Blood, 1 December 2004, Vol. 104, No. 12, pp. 3782-3788. Prepublished online as a Blood First Edition Paper on August 10, 2004; DOI 10.1182/blood-2004-02-0645. This Article Full Text Full Text (PDF) All Versions of this Article: 2004-02-0645v1 104/12/3782    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map 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 Sloand, E. M. Articles by Young, N. S. Search for Related Content PubMed PubMed Citation Articles by Sloand, E. M. Articles by Young, N. S. Related Collections Red Cells Transfusion Medicine Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  TRANSFUSION MEDICINE Transfer of glycosylphosphatidylinositol-anchored proteins to deficient cells after erythrocyte transfusion in paroxysmal nocturnal hemoglobinuria Elaine M. Sloand, Lori Mainwaring, Keyvan Keyvanfar, Jichun Chen, Jaroslaw Maciejewski, Harvey G. Klein, and Neal S. Young From the Hematology Branch, National Heart, Lung, and Blood Institute, and the Department of Transfusion Medicine, Clinical Center, National Institutes of Health, Bethesda, MD. In paroxysmal nocturnal hemoglobinuria (PNH), an acquired mutation of the PIGA gene results in the absence of glycosylphosphatidylinositol (GPI)–anchored cell surface membrane proteins in affected hematopoietic cells. Absence of GPI-anchored proteins on erythrocytes is responsible for their increased sensitivity to complement-mediated lysis, resulting in hemolytic anemia. Cell-to-cell transfer of CD55 and CD59, 2 GPI-anchored proteins, by red cell microvesicles has been demonstrated in vitro, with retention of their function. Because red cell units stored for transfusion contain many erythrocyte microvesicles, transfused blood could potentially serve as a source of CD55 and CD59. We examined whether GPI-anchored proteins could be transferred in vivo to deficient cells following transfusions given to 6 patients with PNH. All patients were group A1 blood type. Each was given transfusions of 3 U of compatible, washed group O blood. Patient group A1 cells were distinguished from the transfused group O cells by flow cytometry and staining with a labeled lectin, Dolichos biflorus, which specifically binds to group A1 erythrocytes. Increased surface CD59 was measured on recipient red cells and granulocytes 1, 3, and 7 days following transfusion in all 6 patients. Our data suggest a potential therapeutic role for GPI-anchored protein transfer for severe PNH. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: C. Metzner, M. M. Mostegl, W. H. Gunzburg, B. Salmons, and J. A. Dangerfield Association of glycosylphosphatidylinositol-anchored protein with retroviral particles FASEB J, August 1, 2008; 22(8): 2734 - 2739. [Abstract] [Full Text] [PDF] S.-M. Chung, O.-N. Bae, K.-M. Lim, J.-Y. Noh, M.-Y. Lee, Y.-S. Jung, and J.-H. Chung Lysophosphatidic Acid Induces Thrombogenic Activity Through Phosphatidylserine Exposure and Procoagulant Microvesicle Generation in Human Erythrocytes Arterioscler. Thromb. Vasc. Biol., February 1, 2007; 27(2): 414 - 421. [Abstract] [Full Text] [PDF]

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