This is supported by in vitro studies showing that DNA-containing ICs from active SLE patients’ serum, activate the innate immune system by inducing pDCs to produce IFN-α, and other pro-inflammatory cytokines and chemokines.30,32 Studies on healthy first-degree relatives of SLE patients have shown elevated serum IFN-α levels compared to healthy unrelated individuals.31,33 suggesting that an underlying genetic susceptibility is also required for producing high IFN-α levels in SLE. This evidence concerns the gene IFNA17 and systemic lupus erythematosus.