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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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IRF3-dependent type I interferon response in B cells regulates CpG-mediated antibody production.

Hypomethylated CpG oligonucleotides (CpG) are not only potent adjuvants for enhancing adaptive immune responses but may also play a critical role in the development of autoimmune diseases such as Rheumatoid Arthritis (RA) and Systemic Lupus Erythematosus (SLE). Here we provide evidence that, in addition to dendritic cells, murine B lymphocytes also exhibit a type I IFN response to CpG-B. Unlike dendritic cells, B cell-mediated type I IFN induction depended on the transcription factor IRF3, but similar to dendritic cells this pathway was independent of the IRF3 kinase TBK1. Utilizing type I IFN receptor-deficient mice, we were able to demonstrate that this IFN pathway enhanced Syndecan-1 expression and IgM production and was required for IgG2a production following CpG-B stimulation. Overall, our findings identify a unique IFN pathway in B cells that may play a central role in mediating B cell biology in response to CpG, potentially implicating this pathway in autoantibody production and the pathogenesis of certain autoimmune diseases.[1]

References

  1. IRF3-dependent type I interferon response in B cells regulates CpG-mediated antibody production. Oganesyan, G., Saha, S.K., Pietras, E.M., Guo, B., Miyahira, A.K., Zarnegar, B., Cheng, G. J. Biol. Chem. (2008) [Pubmed]
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