No evidence for autoimmunity in schizophrenia

A. Schattner*, Y. Cori, T. Hahn, P. Sirota

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

37 Scopus citations


We studied parameters of cellular immunity in 23 schizophrenic patients and compared them to 16 matched healthy controls and to 12 patients with rheumatoid arthritis (RA). None of the patients was receiving neuroleptic drug treatment before the study. We used highly sensitive methods to examine the interferon system by determination of the interferon-induced enzyme 2'-5' oligo-adenylate synthetase [2-5A] in peripheral blood mononuclear cells. Tumor necrosis factor alpha (TNF-α) production was measured in the plasma and in vitro by bioassay of supernatants of stimulated blood cells and of unstimulated cells (spontaneous TNF secretion). In addition, we determined cell-mediated (spontaneous) cytotoxicity, major T cell subsets (CD3, CD4 and CD8 positive cells) and serum neopterin levels. No statistically significant differences could be found between the patients with schizophrenia and the control group in any of the tests used, and no particular subgroup of patients could be identified. In contrast, RA patients had increased serum neopterin and TNF levels, increased LPS-induced TNF production in vitro, increased 2-5A levels and a decrease in CD8 cells associated with an increase in CD4 cells. Thus, in the group of patients studied, we could find no substantiation for the presence of either autoimmune or occult viral cofactors in the pathogenesis of schizophrenia.

Original languageEnglish
Pages (from-to)661-666
Number of pages6
JournalJournal of Autoimmunity
Issue number5
StatePublished - Oct 1996
Externally publishedYes


FundersFunder number
National Institute for Psychobiology in Israel


    • Cell-mediated cytotoxicity
    • Interferon
    • Natural rheumatoid arthritis
    • Oligo-adenylate synthetase
    • Schizophrenia
    • Tumour necrosis factor-α


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