Abstract
Abstract Regulating BCR-mediated adaptive immune responses and subsequent immunoglobulin (Ig) secretion is critical for normal immune function. Defective regulation could lead to chronic inflammation, autoimmunity, or cancer. Several regulatory mechanisms control the threshold for B cell activation and Ig secretion. One mechanism negatively regulates the threshold for BCR activation through coligation of FcγRIIb and subsequent recruitment of SHIP. It was thought that FcγRIIB was the primary mechanism by which humoral responses were terminated. However, mice deficient in FcγRIIb do not exhibit excessive Ig secretion indicating other regulatory mechanisms must exist. We recently identified two additional mechanisms by which immunoglobulin secretion is attenuated during adaptive immunity. First, upon engagement of FcγRIII on dendritic cells by antibody/antigen immune complexes (ICs), dendritic cells secrete soluble mediators that repress BCR-mediated Ig secretion. Second, an autocrine mechanism functions to inhibit Ig secretion wherein B cells stimulated via the BCR with anti-μ or antigen secrete soluble mediators that repress Ig secretion. These data suggest that in addition to FcγRIIb, soluble factors secreted by both dendritic cells and B cells have a critical role in regulating immunoglobulin secretion during BCR-mediated adaptive immune responses. Studies are underway to define the relative importance of these pathways in terminating Ig secretion during adaptive immunity.
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