In vitro, IFN-αR and IFN-γR expression on B cells was elevated after TLR7 stimulation; in vivo, after IFN-γ signaling deletion, the renal pathological progression, GC size, Tfh cells response and antibody formation in TLR7-induced SLE-prone mice were attenuated, indicating that IFN-γ promotes the development of autoreactive B cells and the development of SLE [86]. Here, IFNAR1 is linked to systemic lupus erythematosus.