Neuron-Reactive Antibodies in Systemic Lupus Erythematosus

Abstract

Neuropsychiatric involvement is a frequent clinical problem in systemic lupus erythematosus (SLE), occuring in 25–60% of cases at some time during the course of the illness. As is true of the effects of SLE elsewhere, there are protean manifestations of central nervous system (CNS) dysfunction, but most commonly it presents as seizures or organic brain syndrome with psychosis and/or impaired mentation. Despite advances in understanding some of the mechanisms of tissue damage that affect other organs, the pathogenesis of the diffuse CNS involvement in SLE remains uncertain. Inflammatory destruction of small blood vessels, the major pathogenic mechanism affecting other organs, does not appear to play an important role in the CNS (Ellis and Verity, 1979; Johnson and Richardson, 1968). However, accumulating evidence suggests that auto-antibodies reacting with cell surface molecules, the immune-mediated mechanism responsible for some of the hematological problems in SLE, is also a major contributor to the pathogenesis of much of lupus CNS disease.