Journal
JOURNAL OF IMMUNOLOGY
Volume 175, Issue 6, Pages 3469-3473Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.175.6.3469
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Funding
- NIAID NIH HHS [AI37988] Funding Source: Medline
- NIGMS NIH HHS [5T32GM007240] Funding Source: Medline
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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-kappa B 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.
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