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NA1/NA2 antisera inhibit FcgammaRI- but not FcgammaRII- mediated phagocytosis
B K Flesch1, W Maass, J Neppert
1Institute of Transfusion Medicine, University of Kiel, Germany. flesch@transfusion.uni-kiel.de
Background And Objectives:
Alloantibodies against the granulocyte-specific NA antigens play an important role in alloimmune neonatal neutropenia. As the NA system is located on the FcgammaRIIIb, the influence of NA-specific antibodies on granulocyte function is of special interest.
Materials And Methods:
We tested alloantisera specific for NA1 and NA2 for their ability to influence FcgammaR-mediated phagocytosis of polymorphonuclear neutrophils by use of different FcgammaR-specific targets. Red blood cells coated with human IgG anti-D served as specific targets for FcgammaRI-mediated phagocytosis while mouse IgG1 anti-glycophorin A was used to coat red blood cells (RBCs) to obtain FcgammaRII specific targets. To test for a hypothetical induction of phagocytosis by FcgammaRIIIb we used D-- RBCs coated with human monoclonal anti-D as target cells for unprimed neutrophils.
Results:
Granulocyte phagocytosis was directly induced by FcgammaRI and FcgammaRII but not by FcgammaRIIIb. NA1 alloantisera significantly inhibited FcgammaRI-mediated phagocytosis of IFN-gamma-stimulated neutrophils if the corresponding antigen was expressed. Conversely, NA2 alloantisera inhibited FcgammaRI-mediated phagocytosis in NA2-positive individuals. There was no effect of NA1- and NA2-specific alloantibodies on FcgammaRII-mediated phagocytosis.
Conclusion:
NA-specific alloantisera inhibit the FcgammaRI-induced phagocytosis in primed neutrophils, but they do not significantly inhibit their FcgammaRIIa-specific phagocytosis of mIgG1-coated RBCs.