[Neuropsychiatric lupus and autoantibodies against ionotropic glutamate receptor (NMDAR)].
Almost half of lupus patients will experience neuropsychiatric symptoms during the course of their disease. The etiology of the neuronal damages is still uncertain and probably multiple. Autoantibodies reactive with brain have been postulated to play a role. The observation of pathogenic autoantibodies binding the NR2A and NR2B subunits of the ionotropic glutamate receptor (NMDAR) illustrates this hypothesis. First studies showed that 40% of lupus patients possess serum titers of anti-NR2A/B antibody, but the presence of these autoantibodies is not always associated with the occurrence of neuronal damages or neuropsychiatric symptoms. Nevertheless, their presence is observed in the cerebrospinal fluid (CSF) of one half of the patients suffering from neurolupus. The presence in the serum of these autoantibodies anti-NR2A/B of the NMDAR is preliminary to their presence in the CSF where their deleterious effect is observable. Their entry into the brain is dependent on a breach of the blood brain barrier (BBB). In conclusion, the serum titer of autoantibodies against NR2A/B subunits is an indication of the potential for neuropsychiatric manifestations during the course of the disease.
Cohen-Solal
J F G
JF
Center for Autoimmune and Musculoskeletal Disorders, The Feinstein Institute for Medical Research NS-LIJ, 350, Community Drive, Manhasset, NY 11030, USA. jcohenso@nshs.edu
Diamond
B
B
D001323:Autoantibodies / Q000134:cerebrospinal fluid*; D001812:Blood-Brain Barrier; D003072:Cognition Disorders / Q000209:etiology*; D006801:Humans; D008180:Lupus Erythematosus, Systemic / Q000276:immunology*; D058468:Receptors, Ionotropic Glutamate / Q000276:immunology*
D001323:Autoantibodies; D058468:Receptors, Ionotropic Glutamate