Antineuronal antibodies in neuropsychiatric systemic lupus erythematosus

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Abstract
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.

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