In genetically lupus-predisposed background, high levels of IFN-α (known to be an important player in SLE pathogenesis [37]) induce short-lived plasma cell differentiation and autoantibody production, which is further enhanced by co-stimulatory molecules, Toll-like receptor 9 (TLR9) engagement and BAFF [38]. Here, TLR9 is linked to systemic lupus erythematosus.