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(Journal of Leukocyte Biology. 2002;72:685-691.)
© 2002 by Society for Leukocyte Biology

Stimulation of neutrophil apoptosis by immobilized IgA

Laboratory of Immunology, Institute of Hematologic Research, National Academy of Medicine, and Laboratory of Immunogenetics, Department of Microbiology, Buenos Aires University School of Medicine, Argentina

Correspondence: Jorge Geffner, Laboratorio de Inmunología, IIHEMA, Academia Nacional de Medicina, Pacheco de Melo 3081, 1425 Buenos Aires, Argentina. E-mail: geffnerj{at}fibertel.com.ar

In the current study, we analyzed whether immunoglobulin A (IgA) is able to modulate neutrophil apoptosis. We found that culture of neutrophils on immobilized plasma IgA (iIgAp) or secretory IgA (iIgAs) induced a marked increase in apoptotic rates. By contrast, soluble IgAp, IgAs, or aggregated IgAp exerted no effect. Promotion of apoptosis by iIgA was almost completely prevented by blocking antibodies directed to CD18 or CD11b and was shown to be dependent on the activation of the respiratory burst as suggested by the ability of catalase to prevent apoptosis stimulation; the effect of azide, an heme enzyme inhibitor that significantly increased promotion of apoptosis by iIgA; and the inability of iIgA to stimulate apoptosis of neutrophils isolated from chronic granulomatous disease patients. Stimulation of neutrophil apoptosis by IgA might contribute to the control of inflammatory processes in certain autoimmune diseases such as IgA nephropathy in which tissue deposits of IgA or IgA containing immune complexes are found.

Key Words: human • FcR • immune complexes • secretory • aggregated

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