Thus, we immunized Carabin−/− and control mice with CpG-DNA for the following reasons: 1) CpG-DNA is a TLR9 agonist, which mimics an infectious agent; 2) TLR9 is a known B-cell sensor of dsDNA viruses like EBV and Parvovirus B19, which are linked to SLE flares (McClain et al, 2005); 3) the possible interplay between self-antigen BCR activation and TLR activation (Leadbetter et al, 2002); and finally 4) CpG-DNA is known to induce type I interferon production, which is a key factor for SLE pathogenesis (Baccala et al, 2007; Theofilopoulos et al, 2005). This evidence concerns the gene BCR and systemic lupus erythematosus.