IRF3-dependent Type I Interferon Response in B Cells Regulates CpG-mediated Antibody Production

• DOI: 10.1074/jbc.m704755200
• Publication Date: 2007-10-10T00:53:47Z
• Authors: Gagik Oganesyan; Supriya K. Saha; Eric M. Pietras; Beichu Guo; Andrea K. Miyahira; Brian Zarnegar; Genhong Cheng
• Keywords: IRF3; CpG site; Antibody response; TLR9

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, addition to dendritic cells, murine B lymphocytes exhibit type I IFN response CpG-B. Unlike cell-mediated induction depended on transcription factor IRF3, similar cells this pathway was independent IRF3 kinase TBK1. Utilizing receptor-deficient mice, were able demonstrate that enhanced Syndecan-1 expression IgM production required IgG2a following CpG-B stimulation. Overall, our findings identify unique central mediating cell biology CpG, potentially implicating autoantibody pathogenesis certain diseases.