| First Author | Goodyear CS | Year | 2007 |
| Journal | J Immunol | Volume | 178 |
| Issue | 5 | Pages | 2636-40 |
| PubMed ID | 17312102 | Mgi Jnum | J:144121 |
| Mgi Id | MGI:3830143 | Doi | 10.4049/jimmunol.178.5.2636 |
| Citation | Goodyear CS, et al. (2007) Cutting Edge: Bim is required for superantigen-mediated B cell death. J Immunol 178(5):2636-40 |
| abstractText | To impair B cell clonal regulation, the microbial virulence factor, protein A of Staphylococcus aureus, can interact with evolutionarily conserved BCR-binding sites to induce a form of Fas-independent activation-associated B cell death that results in selective immune tolerance. We now show that this in vivo death pathway is associated with induction of increased transcript and protein levels of Bim, a BH3-only proapoptotic Bcl-2 family protein, which is inhibited by excess B cell-activating factor. An absolute requirement for Bim was documented, since Bim-deficient B cells were protected from in vivo superantigen-induced death and instead underwent persistent massive supraclonal expansion without functional impairment. These studies characterize a BCR-dependent negative clonal selection pathway that has been co-opted by a common bacterial pathogen to induce selective defects in host immune defenses. |
