| First Author | Fischer SF | Year | 2007 |
| Journal | Blood | Volume | 110 |
| Issue | 12 | Pages | 3978-84 |
| PubMed ID | 17720882 | Mgi Jnum | J:149102 |
| Mgi Id | MGI:3847610 | Doi | 10.1182/blood-2007-05-091306 |
| Citation | Fischer SF, et al. (2007) Proapoptotic BH3-only protein Bim is essential for developmentally programmed death of germinal center-derived memory B cells and antibody-forming cells. Blood 110(12):3978-84 |
| abstractText | T cell-dependent B-cell immune responses induce germinal centers that are sites for expansion, diversification, and selection of antigen-specific B cells. During the immune response, antigen-specific B cells are removed in a process that favors the retention of cells with improved affinity for antigen, a cell death process inhibited by excess Bcl-2. In this study, we examined the role of the BH3-only protein Bim, an initiator of apoptosis in the Bcl-2-regulated pathway, in the programmed cell death accompanying an immune response. After immunization, Bim-deficient mice showed persistence of both memory B cells lacking affinity-enhancing mutations in their immunoglobulin genes and antibody-forming cells secreting low-affinity antibodies. This was accompanied by enhanced survival of both cell types in culture. We have identified for the first time the physiologic mechanisms for killing low-affinity antibody-expressing B cells in an immune response and have shown this to be dependent on the BH3-only protein Bim. |
