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(Journal of Leukocyte Biology. 2001;69:233-240.)
© 2001 by Society for Leukocyte Biology

Differential effects of anti-FcRIIIb autoantibodies on polymorphonuclear neutrophil apoptosis and function

Véronique Durand^*, Jacques-Olivier Pers^*, Yves Renaudineau^*, Alain Saraux, Pierre Youinou^* and Christophe Jamin^*

^* Laboratory of Immunology
Department of Rheumatology, Institut de Synergie des Sciences et de la Santé, Brest University Medical School, Brest, France

Correspondence: P. Youinou, M.D., D.Sc., Laboratory of Immunology, Brest University Medical School Hospital, 5 av Foch, F 29 609 Brest Cedex, France. E-mail: youinou{at}univ-brest.fr

Anti-Fc receptor IIIb (FcRIIIb) human autoantibodies (Ab) have been classified previously into three groups, based on the results of an indirect immunofluorescence (IIF) test and an enzyme-linked immunosorbent assay (ELISA): IIF+/ELISA+ (group A), IIF+/ELISA- (group B), and IIF-/ELISA+ (group C) sera. In this study, differential effects between IIF+ autoAb, recognizing cell-bound FcR, and those ELISA+, recognizing only cell-free FcR, were studied on polymorphonuclear neutrophils (PMN). Neither group A nor B autoAb was cytotoxic, although both prolonged the survival of PMN by delaying spontaneous apoptosis. By the same extent, the PMN-binding antisera stimulated the appearance of a CD11b^dim population, following a 12-h incubation. This event was associated with a lowered expression of ß2 integrin molecules, resulting in altered PMN function. Treatment with groups A and B autoAb reduced adhesiveness and respiratory burst. This impairment of the responses was more pronounced when the cells originated from donors NA1+NA1+ rather than donors NA2+NA2+. From our observations, the influences of anti-FcRIIIb autoAb on PMN survival, as well as function and subsequent dysregulation of the inflammatory response, have proven somewhat dependent on their target antigens, as determined by IIF coupled with ELISA and FcRIIIb polymorphism.

Key Words: IIF test • autoimmunity • ELISA • endothelial cells

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