Abstract
Systemic lupus erythematosus (SLE) is a multisystem autoimmune disorder characterized by fluctuating levels of immune response hyperactivity, high serum titers of nucleic antigen-specific autoantibodies, and persistent production of type-I interferon (IFN)1. One route to controlling SLE has been to exploit the properties of T cell lymphocyte costimulation inhibitor (CTLA-4), a selective costimulation inhibitor, which suppresses autoantigen-specific T cell response intensity2.