A mechanism for the suppression of ongoing IgE synthesis.
IgE synthesis from the human plasmacytoma U266/AF-10 was suppressed by addition of IgE immune complexes (IgE-IC). This suppression was isotype-specific as synthesis from other B cell lines was unaffected. Using IgE-IC constructed with a monoclonal antibody that recognizes PS protein-IgE and not ND IgE (the IgE protein made by U266/AF-10), we have shown that this suppression was mediated through the cross-linking of the Fc epsilon receptor.
D000888:Antibodies, Anti-Idiotypic / Q000276:immunology; D000936:Antigen-Antibody Complex / Q000276:immunology*; D002460:Cell Line; D005786:Gene Expression Regulation; D006801:Humans; D007073:Immunoglobulin E / Q000096:biosynthesis* / Q000276:immunology; D007132:Immunoglobulin Isotypes / Q000276:immunology; D007165:Immunosuppression Therapy; D008954:Models, Biological; D010954:Plasmacytoma; D011961:Receptors, Fc / Q000276:immunology; D017455:Receptors, IgE
D000888:Antibodies, Anti-Idiotypic; D000936:Antigen-Antibody Complex; D007132:Immunoglobulin Isotypes; D011961:Receptors, Fc; D017455:Receptors, IgE; C026408:anti-IgE antibodies; D007073:Immunoglobulin E