Because excess IFN-I has been linked to the pathogenesis of SLE19, 20, 21, we explored the contribution of pDCs to the pathogenesis of pristane-induced lupus, in which both TLR7 and IFN signaling are required for the production of auto-Abs and the development of glomerulonephritis40, 41, 42. The gene discussed is TLR7; the disease is systemic lupus erythematosus.