FAS and systemic lupus erythematosus: Lpr and gld mice defective for the Fas signaling pathway develop lymphoadenopathy and splenomegaly and produce a large number of autoantibodies developing a disease that resembles human systemic lupus erythematosus (SLE), clearly demonstrating an essential role for the extrinsic apoptotic pathway in controlling autoreactive T and B cells and the fact that alteration in apoptosis can strongly contribute to autoimmune diseases pathogenesis [152, 153].