Premium
Inhibition of rBet v 1‐induced basophil histamine release with specific immunotherapy ‐induced serum immunoglobulin G: no evidence that FcγRIIB signalling is important
Author(s) -
Ejrnaes A. M.,
Svenson M.,
Lund G.,
Larsen J. N.,
Jacobi H.
Publication year - 2006
Publication title -
clinical and experimental allergy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.462
H-Index - 154
eISSN - 1365-2222
pISSN - 0954-7894
DOI - 10.1111/j.1365-2222.2006.02442.x
Subject(s) - histamine , basophil , immunoglobulin e , immunology , receptor , antibody , blocking antibody , immunoglobulin g , basophil activation , chemistry , allergen , allergy , biology , pharmacology , biochemistry
Summary Background Human basophils and mast cells express the low‐affinity immunoglobulin (Ig)G receptor FcγRIIB. It has previously been shown in artificial model systems that cross‐linking of the high‐affinity IgE receptor FcɛRI and FcγRIIB leads to inhibition of FcɛRI signalling. Objective The aim of the present study was to investigate whether cross‐linking of FcɛRI and FcγRIIB contributes to IgG‐mediated inhibition of histamine release in human basophils in a system using the sera from specific immunotherapy (SIT) patients and the major allergen from birch pollen, Bet v 1. As IgG4 furthermore has been proposed to have special blocking properties, we investigated the significance of IgG subclass specificity for this inhibition. Methods Binding of recombinant Bet v 1–IgG complexes to FcγRII and IgG‐binding activities in the sera from 25 birch pollen‐allergic patients treated with SIT were measured using 125 I‐rBet v 1. Inhibition of basophil histamine release was assessed by incubating washed leucocytes with complexes of rBet v 1–IgG with or without blocking of FcγRII. Results We observed low binding of rBet v 1–IgG complexes to FcγRII, which was negatively correlated with the relative IgG4‐binding activities. Blocking of FcγRII did not reverse the SIT–IgG‐induced inhibition of basophil histamine release. However, IgG‐binding activities correlated significantly with the ability of the SIT sera to inhibit basophil histamine release. Conclusion We suggest that at least in birch pollen SIT, the contribution of FcγRIIB‐mediated inhibitory signalling to SIT–IgG‐induced inhibition of human basophil histamine release is of minor importance. The main contributor to the inhibitory effect of SIT‐induced IgG seems to be blocking of the allergen–IgE interaction.