| First Author | Oganesyan G | Year | 2008 |
| Journal | J Biol Chem | Volume | 283 |
| Issue | 2 | Pages | 802-8 |
| PubMed ID | 17925397 | Mgi Jnum | J:130096 |
| Mgi Id | MGI:3770733 | Doi | 10.1074/jbc.M704755200 |
| Citation | Oganesyan G, et al. (2008) IRF3-dependent type I interferon response in B cells regulates CpG-mediated antibody production. J Biol Chem 283(2):802-8 |
| abstractText | 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. |
