IFN-γ promotes the development of systemic lupus erythematosus through the IFNGR1/2-PSTAT1-TBX21 signaling axis.

Background: Systemic lupus erythematosus (SLE) is a chronic disease that causes inflammation in cartilage and the lining of blood vessels. Emerging evidence implicates IFN-γ as a major effector molecule in SLE during both active and stable stages. Here, we investigated the effects of IFN-γ on cytokines that play an autoimmune disease-promoting role and Th1-versus-Th2 and B cell dualism in SLE patients and mouse models of SLE.