"Type I IFN and IFN-related cytokines and chemokines can induce a favorable immune setting to develop autoimmunity. IFN signature seems to be one of the first steps in the pathogenesis of SLE and other autoimmune diseases [
33] . IFN-α can contribute to the pathogenesis of SLE through various mechanisms, including direct and indirect effects on APCs, T cells, and B cells. IFN-α is largely produced by immature DCs, now known as pDCs, which are stimulated by viruses to produce IFN-α, and this production up-regulates expression of TLR7 by B cells, promotes cell death, increasing the release of certain RNA and DNA autoantigens, and primes pDCs to respond more effectively to immunocomplexes [
34] . Recent studies suggested that hypomethylated plasma DNA might be influential in the pathogenesis of SLE. Bacterial and viral DNA, which are hypomethylated, can induce various immune changes that are similar to those observed in SLE, including activation of TLR9 signaling, leading to the overexpression of type I IFN genes, polyclonal B cell activation, and production of autoantibodies such as anti-DNA antibodies, production of IL-6, and resistance to apoptosis, which potentially allows the survival of autoreactive cells [
35] . Indeed, induction and/or aggravation of SLE are well known to occur after bacterial or viral infection."
