Background

Systemic lupus erythematosus (SLE) is an autoimmune disease in which neuropsychiatric involvement is common but poorly understood. According to the Lupus Research Alliance, “therapy for lupus is empiric and involves a variety of non-specific anti-inflammatory and immunosuppressive agents. While these treatments are frequently beneficial, many patients do not respond adequately and suffer significant side effects.” In neuropsychiatric lupus (NPSLE), a CNS with a compromised blood-brain barrier is targeted by autoimmune antibodies, causing neurological and psychiatric/behavioral manifestations. A major gap in the understanding of NPSLE concerns how molecular autoimmune reactions give rise to the observed phenotypic alterations, and how such alterations can be targeted in therapeutic approaches.