TLR9 and systemic lupus erythematosus: First, pDCs associated with type 1 AIP produce large amounts of type I IFNs upon recognition of TLR9 ligands (CpG) derived from bacteria, whereas NETosis-derived self-DNAs together with DAMPs (anti-microbial peptide LL37 and high mobility group box 1) accelerate type I IFN signaling through activation of TLR7 and/or TLR9 in SLE-associated pDCs (Figure 1B) (5, 6, 10, 18–20).