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 Blood, 15 June 2007, Vol. 109, No. 12, pp. 5355-5362.
Prepublished online as a Blood First Edition Paper on February 22, 2007; DOI 10.1182/blood-2006-11-059899.

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IMMUNOBIOLOGY

IgM and IgA anti-erythrocyte autoantibodies induce anemia in a mouse model through multivalency-dependent hemagglutination but not through complement activation

Lucie Baudino1, Liliane Fossati-Jimack2, Christelle Chevalley1, Eduardo Martinez-Soria1, Marc J. Shulman3, and Shozo Izui1

1 Department of Pathology and Immunology, University of Geneva, Geneva, Switzerland; 2 the Rheumatology Section, Hammersmith Campus, Imperial College School of Medicine, London, United Kingdom; and 3 the Department of Immunology, University of Toronto, Ontario, Canada

By generating IgM and IgA switch variants of the 34-3C IgG2a anti–red blood cell (RBC) autoantibody, we evaluated the pathogenic activity of these 2 isotypes in view of the Fc-associated effector functions (ie, complement activation and polyvalency-dependent agglutination). We found that polymeric forms of 34-3C IgM and IgA anti-RBC autoantibody were as pathogenic as IgG2a, which was the most pathogenic among 4 different IgG subclasses, whereas their monomeric variants completely lacked pathogenic effects. Histological examination showed that 34-3C IgM and IgA autoantibodies caused anemia as a result of multivalency-dependent hemaggultination and subsequent sequestration of RBC in the spleen, in contrast to Fc receptor– and complement receptor–mediated erythrophagocytosis by Kupffer cells with IgG isotypes. In addition, the development of anemia induced by IgM and IgA isotypes of 34-3C antibody and by 2 additional IgM anti-RBC monoclonal autoantibodies was not inhibited at all in C3-deficient mice, indicating the lack of involvement of complement activation in the pathogenesis of IgM- and IgA-induced anemia. Our data demonstrate a remarkably high pathogenic potential of polymeric forms of IgM and IgA anti-RBC autoantibodies due to their ability to induce hemagglutination but completely independent of complement activation.


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