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Blood, 1 January 2007, Vol. 109, No. 1, pp. 155-158. Prepublished online as a Blood First Edition Paper on September 5, 2006; DOI 10.1182/blood-2006-05-023796. This Article Full Text Full Text (PDF) Supplemental Figures All Versions of this Article: blood-2006-05-023796v1 109/1/155    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 Transfusion Medicine Immunotherapy Brief Reports Related Article in Blood Online Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  HEMOSTASIS, THROMBOSIS, AND VASCULAR BIOLOGY Brief report A role for IL-1 receptor antagonist or other cytokines in the acute therapeutic effects of IVIg? Andrew R. Crow, Seng Song, John W. Semple, John Freedman, and Alan H. Lazarus Canadian Blood Services, Department of Laboratory Medicine, St Michael's Hospital, Toronto, ON, Canada; Departments of Pharmacology, Medicine, and Laboratory Medicine and Pathobiology, University of Toronto, ON, Canada; Toronto Platelet Immunobiology Group, ON, Canada The exact mechanism of action of IVIg in the amelioration of immune thrombocytopenic purpura (ITP) is still unclear. Studies have suggested that IVIg may function through the regulation of cytokines, including interleukin-1 receptor antagonist (IL-1Ra), an inhibitor of phagocytosis. Using a mouse model relevant to ITP, we confirm an increase in mouse serum levels of IL-1Ra after exposure to IVIg, yet a recombinant IL-1Ra did not ameliorate thrombocytopenia. IVIg has also been shown to affect the expression of other regulatory cytokines. We have also recently established that IVIg specifically targets activating FcRs on CD11c+ dendritic cells (DCs) as its primary mechanism of action in the amelioration of murine ITP. Herein, we show that IVIg functions therapeutically in mice lacking specific cytokines or their receptors that can potentially affect DC/macrophage function (IL-1 receptor, IL-4, IL-10, IL-12ß, TNF-, IFN- receptor, MIP-1). This suggests that while IVIg may mediate the release of a variety of cytokines, the cytokines tested do not directly participate in the mechanism of IVIg action. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? Related Article in Blood Online: IVIg in ITP: no role for cytokines? Bethan Psaila and James B. Bussel Blood 2007 109: 4-5. [Full Text] [PDF] This article has been cited by other articles: J. Chang, P. A. Shi, E. Y. Chiang, and P. S. Frenette Intravenous immunoglobulins reverse acute vaso-occlusive crises in sickle cell mice through rapid inhibition of neutrophil adhesion Blood, January 15, 2008; 111(2): 915 - 923. [Abstract] [Full Text] [PDF]

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