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Blood, 1 April 2006, Vol. 107, No. 7, pp. 2976-2983. Prepublished online as a Blood First Edition Paper on November 29, 2005; DOI 10.1182/blood-2005-06-2562. This Article Full Text Full Text (PDF) All Versions of this Article: 2005-06-2562v1 107/7/2976    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 Ni, H. Articles by Freedman, J. Search for Related Content PubMed PubMed Citation Articles by Ni, H. Articles by Freedman, J. Related Collections Hemostasis, Thrombosis, and Vascular Biology Transfusion Medicine Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  TRANSFUSION MEDICINE A novel murine model of fetal and neonatal alloimmune thrombocytopenia: response to intravenous IgG therapy Heyu Ni, Pingguo Chen, Christopher M. Spring, Ebrahim Sayeh, John W. Semple, Alan H. Lazarus, Richard O. Hynes, and John Freedman From the Departments of Laboratory Medicine and Pathobiology, Medicine, and Pharmacology, University of Toronto, ON, Canada; The Canadian Blood Services, Ottawa, ON, Canada; The Toronto Platelet Immunobiology Group, St Michael's Hospital, Toronto, ON, Canada; and the Department of Biology, Howard Hughes Medical Institute and Center for Cancer Research, Massachusetts Institute of Technology, Cambridge, MA. Fetal and neonatal alloimmune thrombo cytopenia (FNAITP) is a life-threatening bleeding disorder caused by maternal antibodies directed against fetal platelet antigens. The immunoreactive epitopes in FNAITP are primarily located in the extracellular regions of the platelet glycoprotein IIIa (3 integrin). Here we have established a novel animal model of FNAITP using 3 integrin–deficient (3-/-) mice. We demonstrated first that these mice are immunoresponsive to 3 integrin; 3-/- mice transfused with wild-type platelets generated specific anti–3 antibodies which were able to induce thrombocytopenia in wild-type mice. Subsequently, 3-/- female mice (both naive and immunized) were bred with wild-type male mice to recapitulate the features of FNAITP. The titer of generated maternal antibodies correlated with the severity of FNAITP. High titer maternal anti–3 anti-bodies caused severe fetal thrombocytopenia, intracranial hemorrhage, and even miscarriage. Furthermore, maternal administration of intravenous immunoglobulin G (IgG) ameliorated FNAITP and down-regulated pathogenic antibodies in both the maternal and fetal circulations. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: A. Reheman, H. Yang, G. Zhu, W. Jin, F. He, C. M. Spring, X. Bai, P. L. Gross, J. Freedman, and H. Ni Plasma fibronectin depletion enhances platelet aggregation and thrombus formation in mice lacking fibrinogen and von Willebrand factor Blood, February 19, 2009; 113(8): 1809 - 1817. [Abstract] [Full Text] [PDF]

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