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CUTTING EDGE |
RII-B1 Regulates the Presentation of B Cell Receptor-Bound Antigens1
Department of Cell Biology, Yale University School of Medicine, New Haven, CT 06520
Fc
receptors (FcRII) on B lymphocytes negatively regulate
B cell receptor (BCR)-dependent activation upon cross-linking of the
two receptors. The mechanism reflects the ability of the FcRII
cytoplasmic tail to recruit specific phosphatases that inactivate
elements of the BCR-signaling cascade. We now show that cross-linking
also blocks the processing and presentation of BCR-bound Ag. This
occurs because the FcRII isoform typically expressed by B cells
(FcRII-B1) is incompetent for endocytosis. When cross-linked,
FcRII-B1 acts as a dominant negative inhibitor of BCR endocytosis.
In contrast, cross-linking of endocytosis-competent FcRII isoforms
did not inhibit endocytosis or processing of BCR-bound Ag. Thus,
FcRII-B1 acts not only to prevent B cell activation under conditions
of Ab excess, but also to prevent clonotypic T cell activation by
inhibiting the ability of B cells to generate specific MHC class
II-bound TCR ligands.
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