| First Author | Beisner DR | Year | 2005 |
| Journal | J Immunol | Volume | 175 |
| Issue | 6 | Pages | 3469-73 |
| PubMed ID | 16148088 | Mgi Jnum | J:116713 |
| Mgi Id | MGI:3694859 | Doi | 10.4049/jimmunol.175.6.3469 |
| Citation | Beisner DR, et al. (2005) Cutting edge: innate immunity conferred by B cells is regulated by caspase-8. J Immunol 175(6):3469-73 |
| abstractText | Caspase-8 is an essential component of death receptor-mediated apoptosis. Along with Fas-associated death domain protein, it is also essential for T cell proliferation in response to antigenic or mitogenic stimuli. To determine whether caspase-8 is also required for B cell proliferation, we generated mice with a B cell-specific Casp8 deficiency. Unlike T cells, caspase-8 was not required for Ag receptor-driven proliferation or Ab formation. Rather, Casp8-deficient B cells failed to proliferate in response to dsRNA and LPS, ligands for TLR3 and TLR4, respectively, but responded normally to the TLR9 agonist CpG DNA. Similarly, Ab production to trinitrophenol-LPS was selectively reduced in B cell-specific Casp8-deficient mice. The activation of NF-kappaB or IFN regulatory factor 3 was found to be unaffected by the loss of caspase-8, implicating it in a novel pathway important for some forms of innate immunity mediated by B cells. |
