Th1, Th2 and Th3 cytokine alteration in schizophrenia
Several studies have shown that there is an imbalance between T helper 1 (Th1) cytokines and T helper 2 (Th2) cytokines in patients with schizophrenia. The T helper 3 (Th3) cytokine, transforming growth factor beta-1 (TGF-β1), has been shown to suppress the production of Th1 cytokines. Therefore it...
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Published in | Progress in neuro-psychopharmacology & biological psychiatry Vol. 28; no. 7; pp. 1129 - 1134 |
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Main Authors | , , , , , , |
Format | Journal Article |
Language | English |
Published |
England
Elsevier Inc
01.11.2004
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Subjects | |
Online Access | Get full text |
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Summary: | Several studies have shown that there is an imbalance between T helper 1 (Th1) cytokines and T helper 2 (Th2) cytokines in patients with schizophrenia. The T helper 3 (Th3) cytokine, transforming growth factor beta-1 (TGF-β1), has been shown to suppress the production of Th1 cytokines. Therefore it is hypothesized that it may play a role in schizophrenia by suppressing overactive Th1 system.
We recruited 88 schizophrenic patients and 88 matched controls. The basal plasma concentrations of IFN-γ (Th1), IL-4 (Th2) and TGF-β1 (Th3) were studied at the time the patients were admitted to the hospital and following 8 weeks of treatment with antipsychotics.
The detection rate of plasma IFN-γ and basal plasma TGF-β1 level were significantly higher in schizophrenic patients than in controls whereas detection rate of plasma IL-4 was lower in patients. The ratio of Th1/Th2 cytokines (IFN-γ/IL-4) was higher in schizophrenic patients. Following the neuroleptic treatment, the IFNγ and TGF-β1 levels returned to control values, and IL-4 concentration rose above the control value.
Schizophrenic patients showed higher Th1/Th2 ratio which is attenuated by effective neuroleptic treatment. It is possible that TGF-β1 plays a role in reducing the activity of Th1 cytokine. |
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Bibliography: | ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 23 |
ISSN: | 0278-5846 1878-4216 |
DOI: | 10.1016/j.pnpbp.2004.05.047 |