ISSN:
1433-8491
Keywords:
Schizophrenia
;
Immune system
;
Cytokine Interferon
Source:
Springer Online Journal Archives 1860-2000
Topics:
Medicine
Notes:
Abstract In an attempt to define potential immunological dysfunctions in schizophrenia, we determined the production of interleukin-2 (IL-2), interleukin-4 (IL-4), interferon-γ (IFN-γ), and soluble IL-2 receptor (sIL-2R) in a whole-blood assay after stimulation with phytohemagglutinin (PHA) as well as the serum concentrations of sIL-2R. Because CD4 +CD45RO+T cells are the main producers of IFN-γ, we determined the percentage of these cells, as well as of pan T, CD4+T, and CD8+T cells, by flow cytometry. A whole-blood count was performed in addition. Two groups of patients were examined, paranoid-type and residual-type schizophrenics. The numbers of both monocytes and neutrophils, but not of lymphocytes, were increased significantly in the schizophrenic sample. The IFN-γ production of the schizophrenics as a whole group, and of the paranoid patients, was reduced significantly in comparison with the control group (p≤0.05). The residual patients produced less IFN-γ than the controls, but more than the paranoid patients. The latter differences did not reach statistical significance. The production of IL-4, which physiologically antagonizes the production of IFN-γ, was not significantly higher in the patient group. No changes in the lymphocyte subpopulations were observed. The production of IL-2 showed a trend toward reduction in paranoid patients, but not in residual schizophrenics. The serum sIL-2R levels were elevated slightly in schizophrenics when compared with controls. In order to rule out a possible effect of cortisol on cytokine production, 20 schizophrenic were compared with 20 age- and gendermatched controls. However, neither elevated cortisol levels were detected in the schizophrenic sample, nor significant intercorrelations between cortisol levels and cytokine production, or levels of sIL-2R, respectively. In summary, our data reinforce the possibility of immune dysfunction in schizophrenia and point to the possible relevance of disease subgroups in this respect.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1007/BF02190280
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