Inhibition of B-cell receptor-antigen complex internalization by FcγRIIB1 signals1This work was supported by grants from the Arthritis Society of Canada (96069) and National Cancer Institute of Canada (6349).1

摘要: Abstract Membrane-expressed immunoglobulins are B-cell receptors (BCR) for specific antigens (Ag). Upon Ag engagement of the BCR, B-cells activated to internalize Ag-BCR complexes, process and subsequently present Ag-peptides loaded in class II MHC. Due nature cognate interaction between T-cells expressing Ag-specific T-cell receptor these Ag-presenting occur a highly regulated precise manner. Accordingly, efficient control activation may be achieved through regulation presenting B-cells. A potent form lymphocyte responses is mediated by Ig end-product anti-idiotypic antibodies via Fc-dependent mechanisms. In this communication, authors data that an anti-idiotype (anti-Id) Ab inhibits BCR-mediated internalization Ag. Coupling BCR cytoskeleton was also abortive anti-Id Ab-treated Inhibition dependent upon presence Fc γ RIIB1 on As result suppression, were unable initiate Ca 2+ T-cells. The results suggest co-crosslinking cytoskeletal coupling complex thereby preventing presentation Anti-Id mediate negative regulatory mechanism suppresses B-cell-mediated activation.