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  • Title: Cutting Edge: Bim is required for superantigen-mediated B cell death.
    Author: Goodyear CS, Corr M, Sugiyama F, Boyle DL, Silverman GJ.
    Journal: J Immunol; 2007 Mar 01; 178(5):2636-40. PubMed ID: 17312102.
    Abstract:
    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.
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