Monocytic, Th1 and Th2 cytokine alterations in the pathophysiology of schizophrenia

Kyeong Sae Na, Yong Ku Kim

Research output: Contribution to journalArticle

62 Citations (Scopus)

Abstract

A growing body of evidence suggests that changes in the serum levels and cellular production of various cytokines are associated with the immunological abnormalities of schizophrenia. Several studies have examined alterations in T helper type 1 (Th1) and T helper type 2 (Th2) cytokines in schizophrenia. We explored monocytic, Th1 and Th2 cytokines in 43 schizophrenia patients and 50 normal controls. The mitogen-induced production of tumor necrosis factor α (TNF-α), interleukin 6 (IL-6), IL-4, γ-interferon (IFN-γ) and IL-2 was measured with enzyme-linked immunosorbent assays before and after antipsychotic treatment. IL-6 and TNF-α production by schizophrenic patients was significantly higher than by normal controls, while IL-2, IL-4 and IFN-γ production was significantly lower in schizophrenic patients. After 6 weeks of antipsychotic treatment, IL-6 and TNF-α production was significantly decreased, while IL-4, IFN-γ and IL-2 productions were not significantly changed. Our results suggest that increased monocytic cytokines and decreased Th1 and Th2 cytokines may be associated with the immunopathogenesis of acute psychotic schizophrenia, and that antipsychotics may play an important role in immune response by decreasing elevated monocytic cytokines.

Original languageEnglish
Pages (from-to)55-63
Number of pages9
JournalNeuropsychobiology
Volume56
Issue number2-3
DOIs
Publication statusPublished - 2008 Feb

Keywords

  • Antipsychotics
  • Cytokines
  • Interferons
  • Interleukins
  • Psychoimmunology
  • Schizophrenia

ASJC Scopus subject areas

  • Neuropsychology and Physiological Psychology
  • Psychiatry and Mental health
  • Biological Psychiatry

Fingerprint Dive into the research topics of 'Monocytic, Th1 and Th2 cytokine alterations in the pathophysiology of schizophrenia'. Together they form a unique fingerprint.

  • Cite this