The past year has seen advances in our understanding of accessory membrane proteins that modulate the B cell response to antigen-receptor stimulation. The generation of complement receptor deficient mice has reinforced our appreciation of the importance of complement receptors in the B cell response to antigen. The association of inositol polyphosphate 5-phosphatase with FcgammaRIIB suggests another mechanism, in addition to recruitment of the phosphotyrosine phosphatase SHP-1, by which secreted immunoglobulin can limit further response to antigen. The in vivo function of CD22 in regulating the threshold of antigen-receptor signalling has been shown using CD22-deficient mice. Lastly, B cell receptor signalling in the B-1 subset of B lymphocytes has been demonstrated to be negatively regulated by CD5.