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Blood, 15 February 2005, Vol. 105, No. 4, pp. 1546-1548. Prepublished online as a Blood First Edition Paper on October 12, 2004; DOI 10.1182/blood-2004-05-1886. This Article Full Text Full Text (PDF) Supplemental Figures All Versions of this Article: 2004-05-1886v1 105/4/1546    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 Song, S. Articles by Lazarus, A. H. Search for Related Content PubMed PubMed Citation Articles by Song, S. Articles by Lazarus, A. H. Related Collections Brief Reports Hemostasis, Thrombosis, and Vascular Biology Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  HEMOSTASIS, THROMBOSIS, AND VASCULAR BIOLOGY Brief report Monoclonal antibodies that mimic the action of anti-D in the amelioration of murine ITP act by a mechanism distinct from that of IVIg Seng Song, Andrew R. Crow, Vinayakumar Siragam, John Freedman, and Alan H. Lazarus From the Transfusion Medicine Research, St Michael's Hospital; The Canadian Blood Services; and The Toronto Platelet Immunobiology Group, Toronto, ON, Canada. The mechanism of action of intravenous immunoglobulin (IVIg) and polyclonal anti-D–mediated reversal of immune thrombocytopenia (ITP) is still unclear. However, in a murine model of ITP, the therapeutic effect of IVIg appears to be wholly dependent upon the expression of the inhibitory Fc receptor, FcRIIB. We previously demonstrated that, similar to anti-D in humans, 2 erythrocyte-reactive monoclonal antibodies (TER119 and M1/69) ameliorated murine ITP and inhibited reticuloendothelial system (RES) function at doses that protected against thrombocytopenia. The current study evaluated the involvement of the inhibitory and activating Fc receptors, FcRIIB and FcRIIIA, respectively, in the TER119 and M1/69-mediated inhibition of thrombocytopenia. In contrast to IVIg, in FcRIIB-deficient mice, both monoclonal antibodies ameliorated ITP and both significantly down-regulated the level of expression of the activating FcRIIIA in splenic macrophages. These results indicate that anti-erythrocyte antibodies that ameliorate ITP act independently of FcRIIB expression but are dependent upon the activating FcRIIIA. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: Y. Li, M. E. Williams, J. B. Cousar, A. W. Pawluczkowycz, M. A. Lindorfer, and R. P. Taylor Rituximab-CD20 Complexes Are Shaved from Z138 Mantle Cell Lymphoma Cells in Intravenous and Subcutaneous SCID Mouse Models J. Immunol., September 15, 2007; 179(6): 4263 - 4271. [Abstract] [Full Text] [PDF] A. R. Crow, S. Song, J. W. Semple, J. Freedman, and A. H. Lazarus A role for IL-1 receptor antagonist or other cytokines in the acute therapeutic effects of IVIg? Blood, January 1, 2007; 109(1): 155 - 158. [Abstract] [Full Text] [PDF] D. B. Cines and J. B. Bussel How I treat idiopathic thrombocytopenic purpura (ITP) Blood, October 1, 2005; 106(7): 2244 - 2251. [Full Text] [PDF]

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