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Differential effects of anti‐FcγRIIIb autoantibodies on polymorphonuclear neutrophil apoptosis and function
Author(s) -
Durand Véronique,
Pers JacquesOlivier,
Renaudineau Yves,
Saraux Alain,
Youinou Pierre,
Jamin Christophe
Publication year - 2001
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1189/jlb.69.2.233
Subject(s) - iif , biology , autoantibody , granulocyte , respiratory burst , apoptosis , immunology , microbiology and biotechnology , immunofluorescence , antigen , receptor , antibody , biochemistry
Anti‐Fcγ receptor IIIb (FcγRIIIb) 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 FcγR, and those ELISA+, recognizing only cell‐free FcγR, 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 β2 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‐FcγRIIIb 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 FcγRIIIb polymorphism.