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Blood, 15 December 2006, Vol. 108, No. 13, pp. 4255-4259. Prepublished online as a Blood First Edition Paper on August 10, 2006; DOI 10.1182/blood-2006-05-021568. This Article Full Text Full Text (PDF) All Versions of this Article: blood-2006-05-021568v1 108/13/4255    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 von Gunten, S. Articles by Simon, H.-U. Search for Related Content PubMed PubMed Citation Articles by von Gunten, S. Articles by Simon, H.-U. Related Collections Immunobiology Transfusion Medicine Immunotherapy Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  TRANSFUSION MEDICINE Immunologic and functional evidence for anti–Siglec-9 autoantibodies in intravenous immunoglobulin preparations Stephan von Gunten, Alexander Schaub, Monique Vogel, Beda M. Stadler, Sylvia Miescher, and Hans-Uwe Simon From the Departments of Pharmacology and Immunology, University of Bern, Bern; and ZLB Behring, Bern, Switzerland. Human intravenous immunoglobulin (IVIg) preparations are increasingly used for the treatment of autoimmune diseases. Earlier work demonstrated the presence of autoantibodies against Fas in IVIg, suggesting that IVIg might be able to induce caspase-dependent cell death in Fas-sensitive cells. In this study, we demonstrate that sialic acid–binding Ig-like lectin 9 (Siglec) represents a surface molecule on neutrophils that is activated by IVIg, resulting in caspase-dependent and caspase-independent forms of cell death. Neutrophil death was mediated by naturally occurring anti–Siglec-9 autoantibodies present in IVIg. Moreover, the efficacy of IVIg-mediated neutrophil killing was enhanced by the proinflammatory cytokines granulocyte/macrophage colony-stimulating factor (GM-CSF) and interferon- (IFN–), and this additional cell death required reactive oxygen species (ROSs) but not caspases. Anti– Siglec-9 autoantibody–depleted IVIg failed to induce this caspase-independent neutrophil death. These findings contribute to our understanding of how IVIg preparations exert their immunoregulatory effects under pathologic conditions and may provide a possible explanation for the neutropenia that is sometimes seen in association with IVIg therapy. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: A. Daryadel, S. Yousefi, D. Troi, I. Schmid, J. Schmidt-Mende, C. Mordasini, C. A. Dahinden, A. Ziemiecki, and H.-U. Simon RhoH/TTF Negatively Regulates Leukotriene Production in Neutrophils J. Immunol., May 15, 2009; 182(10): 6527 - 6532. [Abstract] [Full Text] [PDF] S. Khan and W. A.C. Sewell Risks of Intravenous Immunoglobulin in Sepsis Affect Trial Design Ann Intern Med, December 4, 2007; 147(11): 813 - 813. [Full Text] [PDF]

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