Recent evidence suggests that innate immune activation might directly contribute to detrimental antibody production, as increased TLR7 signaling has been observed to favor differentiation of lupus-associated CD27−IgD− B cells into plasma cells excreting autoreactive antibodies, although co-stimulation by IL-21 and IFN- γ along with TLR7 is required to differentiate naïve B cells into these double negative and plasma cells. Here, TLR7 is linked to systemic lupus erythematosus.