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Prepublished online as a Blood First Edition Paper on March 20, 2003; DOI 10.1182/blood-2003-01-0023. This Article Full Text Full Text (PDF) All Versions of this Article: 2003-01-0023v1 102/2/558    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 Crow, A. R. Articles by Lazarus, A. H. Search for Related Content PubMed PubMed Citation Articles by Crow, A. R. Articles by Lazarus, A. H. Related Collections Hemostasis, Thrombosis, and Vascular Biology Immunobiology Phagocytes Apoptosis Signal Transduction Immunotherapy Brief Reports Related Letter in Blood Online Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Blood, 15 July 2003, Vol. 102, No. 2, pp. 558-560 HEMOSTASIS, THROMBOSIS, AND VASCULAR BIOLOGY Brief report IVIg-mediated amelioration of murine ITP via FcRIIB is independent of SHIP1, SHP-1, and Btk activity Andrew R. Crow, Seng Song, John Freedman, Cheryl D. Helgason, R. Keith Humphries, Katherine A. Siminovitch, and Alan H. Lazarus From the Transfusion Medicine Research, St Michael's Hospital, Toronto, ON, Canada; Canadian Blood Services, Toronto, ON, Canada; Department of Cancer Endocrinology and Terry Fox Laboratory, British Columbia Cancer Agency, Vancouver, BC, Canada; Samuel Lunenfeld Research Institute, Mt Sinai Hospital, Toronto, ON, Canada; and Toronto Platelet Immunobiology Group, Toronto, ON, Canada. It has been established that amelioration of murine immune thrombocytopenia purpura (ITP) by IVIg is dependent on the inhibitory receptor FcRIIB. Co-cross-linking of the FcRIIB with the B-cell receptor complex or with FcRI in mast cells results in cell inhibition, which is mediated by recruitment of the inositol phosphatase SHIP1 to the cytoplasmic tail of the FcR. The FcRIIB can also associate with protein tyrosine phosphatase SHP-1 as a potential secondary target of the receptor. Alternatively, homoaggregation of FcRIIB can induce a proapoptotic state in B cells that is dependent on the presence of Bruton tyrosine kinase (Btk), a kinase also expressed in monocytes. We sought to determine if these signaling pathways may direct IVIg-mediated FcRIIB-dependent regulation of in vivo monocyte function in a murine model of ITP in which IVIg functions in an FcRIIB-dependent manner. We demonstrate that mice deficient in SHIP1, SHP-1, and Btk respond to the ameliorating effects of IVIg with the same kinetics as control mice. We conclude that IVIgmediated inhibitory pathways operating via monocyte FcRIIB may involve a transmembrane signaling pathway different from that of B cells. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? Related Letter in Blood Online: IVIg-mediated amelioration of murine ITP via FcRIIb is not necessarily independent of SHIP-1 and SHP-1 activity Edwin van Mirre, Annet van Royen, C. Erik Hack, Andrew R. Crow, Seng Song, John Freedman, Cheryl D. Helgason, R. Keith Humphries, Katherine A. Siminovitch, and Alan H. Lazarus Blood 2004 103: 1973-1974. [Full Text] [PDF] This article has been cited by other articles: F. Nimmerjahn and J. V. Ravetch The antiinflammatory activity of IgG: the intravenous IgG paradox J. Exp. Med., January 22, 2007; 204(1): 11 - 15. [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] V. Gill, C. Doig, D. Knight, E. Love, and P. Kubes Targeting Adhesion Molecules as a Potential Mechanism of Action for Intravenous Immunoglobulin Circulation, September 27, 2005; 112(13): 2031 - 2039. [Abstract] [Full Text] [PDF] M. Olsson, P. Bruhns, W. A. Frazier, J. V. Ravetch, and P.-A. Oldenborg Platelet homeostasis is regulated by platelet expression of CD47 under normal conditions and in passive immune thrombocytopenia Blood, May 1, 2005; 105(9): 3577 - 3582. [Abstract] [Full Text] [PDF] S. Song, A. R. Crow, V. Siragam, J. Freedman, and A. H. Lazarus Monoclonal antibodies that mimic the action of anti-D in the amelioration of murine ITP act by a mechanism distinct from that of IVIg Blood, February 15, 2005; 105(4): 1546 - 1548. [Abstract] [Full Text] [PDF] E. van Mirre, A. van Royen, C. E. Hack, A. R. Crow, S. Song, J. Freedman, C. D. Helgason, R. K. Humphries, K. A. Siminovitch, and A. H. Lazarus IVIg-mediated amelioration of murine ITP via Fc{gamma}RIIb is not necessarily independent of SHIP-1 and SHP-1 activity Blood, March 1, 2004; 103(5): 1973 - 1974. [Full Text] [PDF]

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