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This Article Full Text Full Text (PDF) 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 Meyer, D. Articles by Gessner, J. E. Search for Related Content PubMed PubMed Citation Articles by Meyer, D. Articles by Gessner, J. E. Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Blood, Vol. 92 No. 11 (December 1), 1998: pp. 3997-4002 RAPID COMMUNICATION FcRIII (CD16)-Deficient Mice Show IgG Isotype-Dependent Protection to Experimental Autoimmune Hemolytic Anemia Dirk Meyer, Carsten Schiller, Jürgen Westermann, Shozo Izui, Wouter L. W. Hazenbos, J. Sjef Verbeek, Reinhold E. Schmidt, and J. Engelbert Gessner From the Departments of Clinical Immunology and Functional Anatomy, Hannover Medical School, Hannover, Germany; the Department of Pathology, CMU, University of Geneva, Geneva, Switzerland; and the Department of Immunology, University Hospital Utrecht, Utrecht, The Netherlands. In autoimmune hemolytic anemia (AIHA), there is accumulating evidence for an involvement of FcR expressed by phagocytic effector cells, but demonstration of a causal relationship between individual FcRs and IgG isotypes for disease development is lacking. Although the relevance of IgG isotypes to human AIHA is limited, we could show a clear IgG isotype dependency in murine AIHA using pathogenic IgG1 (105-2H) and IgG2a (34-3C) autoreactive anti-red blood cell antibodies in mice defective for FcRIII, and comparing the clinical outcome to those in wild-type mice. FcRIII-deficient mice were completely resistent to the pathogenic effects of 105-2H monoclonal antibody, as shown by a lack of IgG1-mediated erythrophagocytosis in vitro and in vivo. In addition, the IgG2a response by 34-3C induced a less severe but persistent AIHA in FcRIII knock-out mice, as documented by a decrease in hematocrit. Blocking studies indicated that the residual anemic phenotype induced by 34-3C in the absence of FcRIII reflects an activation of FcRI that is normally coexpressed with FcRIII on macrophages. Together these results show that the pathogenesis of AIHA through IgG1-dependent erythrophagocytosis is exclusively mediated by FcRIII and further suggest that FcRI, in addition to FcRIII, contributes to this autoimmune disease when other IgG isotypes such as IgG2a are involved. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: A. Braun, J. E. Gessner, D. Varga-Szabo, S. N. Syed, S. 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