IFNAR2 and systemic lupus erythematosus: Systemic lupus erythematosus (SLE) is characterized by autoantigen-deriven interactions between autoreactive Th and B cells, spawning production of somatically mutated IgG autoautibodies against apoptotic nuclear antigens (Ags) [1], [2], pathogenic IgG autoantibodies belonging to Th1- or interferon gamma (IFNr)-dependent subclass contributing differentiation of autoimmune Th cell with concomitant decrease in regulatory T (Treg) cells [3].