Shannon Jones
| Student: Shannon Jones |
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| Undergraduate Institution: | Winston Salem State University |
| Email: | jushanno@email.unc.edu |
| Department: | Toxicology |
| PI: | Barbara Vilen |
| Research Summary: | Regulating BCR-mediated adaptive immune responses and subsequent immunoglobulin (Ig) secretion is critical for normal immune function. Defective regulation could lead to chronic inflammatory diseases,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 Fc?RIIb and subsequent recruitment of SHIP. It was thought that Fc?RIIB was the primary mechanism by which humoral responses were terminated. However, mice deficient in Fc?RIIb do not exhibit excessive Ig secretion indicating other regulatory mechanisms must exist. Our lab has been interested in understanding the role of dendritic cells and macrophages in regulating immunoglobulin secretion. We recently identified two additional mechanisms by which immunoglobulin secretion is attenuated during adaptive immunity. First,upon engagement of Fc?RIII 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-? or antigen secrete soluble mediators that repress Ig secretion. These data suggest that in addition to Fc?RIIb, 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 identify the soluble factors so that genetic studies can define the relative importance of these pathways in attenuating Ig secretion during late stages of the adaptive immune response. |
