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Fcγ receptor II dependency of enhanced presentation of major histocompatibility complex class II peptides by a B cell lymphoma
Author(s) -
Berg Matthias,
Uellner Ruth,
Langhorne Jean
Publication year - 1997
Publication title -
european journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.272
H-Index - 201
eISSN - 1521-4141
pISSN - 0014-2980
DOI - 10.1002/eji.1830270432
Subject(s) - biology , internalization , endocytosis , antigen presentation , antigen , antibody , microbiology and biotechnology , b cell receptor , b cell , receptor , epitope , major histocompatibility complex , cell , antigen presenting cell , t cell , immune system , immunology , biochemistry
Abstract Here we show that the B cell lymphoma A20.292 is capable of enhanced antigen presentation to CD4 + T cells in the presence of specific antibodies. This enhancement was inhibited by anti‐Fcγ receptor (R) antibodies, suggesting that it might be due to preferential uptake of the antigen/antibody complex through the FcγRII receptor. However, immunoprecipitation studies revealed that the FcR of A20.292 cells was of the B cell type, FcγRIIb1, which is not thought to be able to internalize antigen/antibody complexes via clathrin‐coated pits. It was considered unlikely that A20.292 had an altered form of the B cell FcγR (RIIb1) receptor that enabled internalization, since similar enhancing effects were also observed using an FcγRII − cell line that had been transfected with FcγRIIb1. To reconcile these findings with the expression of FcγRIIb1, it is postulated that immune complexes are concentrated on the cell surface by the FcγRIIb1 and are thus available for preferential uptake by random fluid‐phase endocytosis. This results in more efficient generation of the epitopes recognized by these T cell hybridomas.