Antineuronal antibodies in neuropsychiatric systemic lupus erythematosus.
The diagnosis of neuropsychiatric systemic lupus erythematosus (NP-SLE) is clinical and one of exclusion. Brain cross-reactive lymphocytotoxins or neuronal antibodies have been proposed as a mechanism underlying NP-SLE. We assessed the clinical relevance of neuronal cell binding antibodies using a standardized clinical definition of NP-SLE. Serum from 54 SLE patients and 77 controls were tested for binding to 3 neuroblastoma and 3 glioblastoma cell lines. Thirty-three SLE patients (61%) fulfilled clinical criteria for the diagnosis of NP-SLE; of these, 55% had serum binding activity to both neuroblastoma and glioblastoma cell lines, compared with 33% of the other SLE patients. When reactivity to neuroblastoma cell lines only was assessed, 43% of NP-SLE patient sera demonstrated binding activity, versus 14% of sera from the remaining SLE patients. Control subjects' reactivity to neuroblastoma cell lines was positive in 12% of sera. Analysis of serum reactivity using non-neuronal cell lines revealed that neuroblastoma, but not glioblastoma, cell binding was specific. NP-SLE patients with evidence of diffuse symptomatology had a higher mean titer of neuroblastoma cell line binding than those with focal symptomatology. Using a panel of substrates, one can identify a significant proportion of patients who are independently defined as having NP-SLE, who demonstrate specific serum neuronal antibodies.
D001323:Autoantibodies / Q000032:analysis*; D002460:Cell Line; D005910:Glioma / Q000276:immunology; D006801:Humans; D008180:Lupus Erythematosus, Systemic / Q000276:immunology*; D009420:Nervous System / Q000276:immunology*; D009422:Nervous System Diseases / Q000276:immunology*; D009447:Neuroblastoma; D019965:Neurocognitive Disorders / Q000276:immunology*; D009474:Neurons / Q000276:immunology
D001323:Autoantibodies