WAS and nephritis: Consistent with the B6.Nba2 and WAS models, T1IFN signaling was also not required for TLR7-driven nephritis in NZM2328 lupus-prone mice [67], although we observed a moderate reduction in TLR7-mediated autoimmune B cell responses, immune complex deposition, and nephritis in B6.Sle1b mice [63].