In a separate study, we conditionally deleted IFNγR in B cells in a TLR7-induced B6.Sle1b SLE disease model and found that B cell-intrinsic IFNγ signaling was necessary and sufficient for promoting splenomegaly, elevated GC, AFC, Tfh, and autoantibody responses, and for the development of lupus nephritis [63]. Here, IFNG is linked to lupus nephritis.