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HMGB1‐mediated microglial activation as a mechanism for cognitive dysfunction in neuropsychiatric lupus

Systemic Lupus Erythematosus (SLE) is an autoimmune disease characterized by the presence of anti‐nuclear antibodies as well as a broad array of clinical manifestations spanning nearly every organ system. Neuropsychiatric syndromes affect over one half of SLE patients, presenting most commonly as cognitive dysfunction or headache. The pathophysiology of neuropsychiatric lupus is not fully understood; however, a critical mechanism has been identified, which involves passage of inflammatory cytokines and anti‐brain antibodies through the blood‐brain barrier.