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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 (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 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 Related Letter in Blood Online Social Bookmarking                   What's this? Submitted January 6, 2003 Accepted March 12, 2003 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* Transfusion Medicine Research, St Michael's Hospital, Toronto, ON, Canada Canadian Blood Services, Canada Cancer Endocrinology, British Columbia Cancer Agency, Vancouver, BC, Canada Terry Fox Laboratory, British Columbia Cancer Agency, Vancouver, BC, Canada Samuel Lunenfeld Research Institute, Mt. Sinai Hospital, Toronto, ON, Canada * Corresponding author; email: lazarusa{at}smh.toronto.on.ca. It has been established that amelioration of murine ITP by IVIg is dependent upon the inhibitory receptor FcRIIB. Co-crosslinking 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 upon the presence of Bruton's 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 SHIP1, SHP-1 and Btk deficient mice respond to the ameliorating effects of IVIg with the same kinetics as control mice. We conclude that IVIg-mediated 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: Y. Zhang, S. Liu, J. Liu, T. Zhang, Q. Shen, Y. Yu, and X. Cao Immune Complex/Ig Negatively Regulate TLR4-Triggered Inflammatory Response in Macrophages through Fc{gamma}RIIb-Dependent PGE2 Production J. Immunol., January 1, 2009; 182(1): 554 - 562. [Abstract] [Full Text] [PDF] N. Dussault, E. Ducas, C. Racine, A. Jacques, I. Pare, S. 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