Production of interferons and lymphokines in leukocyte cultures of patients with schizophrenia

Hörnberg, Maria; Arolt, Volker; Wilke, I.; Kruse, Andrea; Kirchner, Holger

doi:10.1016/0920-9964(94)00046-b

Cited by 86 publications

(31 citation statements)

References 22 publications

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“…Our results confirm the association between acute schizophrenia and low IL-2 production, [8][9][10][11][12][13][14][15] but also clearly confirm our earlier results 30 which showed a decreased IFN-␥ production in acute schizophrenia. Deficient lymphocyte productions of both IL-2 and IFN-␥ were also found throughout the time period of clinical remission, which were also significantly intercorrelated with one another at all three time-points of the investigation.…”

Section: Discussionsupporting

confidence: 82%

“…Six different groups, including our own, have independently demonstrated that mitogen stimulated IL-2 production by peripheral blood mononuclear cells (PBMC) is decreased in patients with schizophrenia. [8][9][10][11][12][13][14][15] This is the most frequently confirmed finding in the immunology of schizophrenia and there has not as yet been a failure in demonstrating this phenomenon. In the cerebrospinal fluid (CSF) of drug-free patients, increased levels of IL-2 were found 16 and also significantly predicted the recurrence of psychotic symptoms in relapse-prone schizophrenics.…”

Section: Introductionmentioning

confidence: 99%

“…It is therefore likely that in vitro stimulation effects better reflect actual in vivo cytokine production by immunocompetent cells. Using the same methods as were used in our pilot study, 14 we have demonstrated a significantly reduced production of IFN-␥ in an acutely ill subsample of a larger group of patients with schizophrenia. 15 Recently this finding could be confirmed in samples of hospitalized acutely psychotic schizophrenics 29 and in acutely schizophrenic members of multiplex families.…”

Section: Introductionmentioning

confidence: 99%

“…Whilst there is some evidence that the mean serum levels of IFN-␥ in schizophrenics (except in one report) 20 resemble those of normal controls, [21][22][23] the production of IFN-␥ after mitogenic stimulation was only mildly and on the whole not significantly decreased in schizophrenia, 14,[24][25][26] although one study did find a significant decrease. 27 The lack of coherence in these results can be explained by the fact that studies varied considerably with respect to the use of bioassays, cell preparation techniques, and also recruitment of patients.…”

Section: Introductionmentioning

confidence: 99%

“…17 Elevated levels of the sIL-2R in peripheral blood, a sign that also indicates lymphocyte activation, were also repeatedly observed in schizophrenia. 14,18,19 Hence concerning cytokines and their role as indicators for T-cell activation, there are impressive parallels between autoimmune disorders and schizophrenia.…”

Section: Introductionmentioning

confidence: 99%

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Decreased in vitro production of interferon-gamma and interleukin-2 in whole blood of patients with schizophrenia during treatment

et al. 2000

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A pattern of aberrations in the T-cell cytokine system that is typical for autoimmune disorders has also been reported in patients with schizophrenia, namely a decreased interleukin-2 (IL-2) production and increased levels of the soluble IL-2 receptor (sIL-2R). It has also been reported that the production of interferon-␥ (IFN-␥) may be lowered. In a longitudinal design, we studied the production of both IFN-␥ and IL-2 and their correlation in patients with schizophrenia during treatment and investigated whether associations exist between cytokine production and clinical variables. The production of IFN-␥ and IL-2 was measured in equal numbers (n = 29) of patients with schizophrenia (DSM-IV) and controls who were matched for age and gender. Patients were measured 1 day after admission (T1), after 14 (T2) and 28 (T2) days of treatment. Psychopathology was assessed after these times. The production of both IFN-␥ and IL-2 was significantly lower in patients than in controls throughout the whole investigation period (T1-T3). The productions of both cytokines were significantly correlated in controls (r = 0.60, P Յ 0.001) as well as in patients with schizophrenia (mean production T1-T3: r = 0.71, P Յ 0.001). No associations between cytokine measurements and psychopathology or age-at-onset could be found. Our findings of lowered and correlated IFN-␥ and IL-2 production indicate that alterations in the cytokine system of patients with schizophrenia might resemble those in autoimmune disorders. It is suggested that these immunological abnormalities are associated with acute exacerbation, rather than with a clinical subtype of schizophrenia. Molecular Psychiatry (2000) 5, 150-158.

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Section: Discussionsupporting

confidence: 82%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Decreased in vitro production of interferon-gamma and interleukin-2 in whole blood of patients with schizophrenia during treatment

et al. 2000

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A Neuroimmunological Model of Schizophrenia and Major Depression: A Review

Holden

Pakula

Mooney

1997

Hum. Psychopharmacol. Clin. Exp.

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In this paper the neuroimmunology of schizophrenia and major depression will be reviewed. The causal role the neuropeptides, cytokines and insulin play in the pathogenesis of positive and negative schizophrenia and major depression will be examined. Numerous studies have shown there is an intimate interaction between certain cytokines and neuropeptides, possibly because the neuropeptides are exclusively synthesized in immune cells. When this relationship is dysregulated, a self‐perpetuating pathobiochemical network is established that becomes difficult to reverse. This disruption to normal metabolism also involves insulin which becomes dysregulated by the inflammatory cytokines: interleukin‐1 (IL‐1), IL‐6, tumour necrosis factor‐alpha (TNF‐α) and interferon‐gamma (IFN‐γ). Each of these cytokines can independently inhibit and/or increase insulin secretion, but they can also function synergistically, which compounds the influence on insulin secretion. An hypothesis is proposed that: (i) when brain insulin is elevated, energy metabolism and neurotransmission is hyperactive resulting in the positive symptoms of schizophrenia; and (ii) when brain insulin is inhibited, energy metabolism and neurotransmission is hypoactive resulting in either the negative symptoms of schizophrenia or major depression. It is our intention to develop a neuroimmunological model of positive and negative schizophrenia and major depression based on the causal interaction between the neuropeptides, the inflammatory cytokines and insulin. © 1997 John Wiley & Sons, Ltd.

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A Neuroimmunological Model of Schizophrenia and Major Depression: A Review

Holden

Pakula

Mooney

1997

Hum. Psychopharmacol. Clin. Exp.

View full text Add to dashboard Cite

In this paper the neuroimmunology of schizophrenia and major depression will be reviewed. The causal role the neuropeptides, cytokines and insulin play in the pathogenesis of positive and negative schizophrenia and major depression will be examined. Numerous studies have shown there is an intimate interaction between certain cytokines and neuropeptides, possibly because the neuropeptides are exclusively synthesized in immune cells. When this relationship is dysregulated, a self-perpetuating pathobiochemical network is established that becomes dicult to reverse. This disruption to normal metabolism also involves insulin which becomes dysregulated by the in¯ammatory cytokines: interleukin-1 (IL-1), IL-6, tumour necrosis factor-alpha (TNF-a) and interferon-gamma (IFN-g). Each of these cytokines can independently inhibit and/or increase insulin secretion, but they can also function synergistically, which compounds the in¯uence on insulin secretion. An hypothesis is proposed that: (i) when brain insulin is elevated, energy metabolism and neurotransmission is hyperactive resulting in the positive symptoms of schizophrenia; and (ii) when brain insulin is inhibited, energy metabolism and neurotransmission is hypoactive resulting in either the negative symptoms of schizophrenia or major depression. It is our intention to develop a neuroimmunological model of positive and negative schizophrenia and major depression based on the causal interaction between the neuropeptides, the in¯ammatory cytokines and insulin.

show abstract

Production of interferons and lymphokines in leukocyte cultures of patients with schizophrenia

Cited by 86 publications

References 22 publications

Decreased in vitro production of interferon-gamma and interleukin-2 in whole blood of patients with schizophrenia during treatment

Decreased in vitro production of interferon-gamma and interleukin-2 in whole blood of patients with schizophrenia during treatment

A Neuroimmunological Model of Schizophrenia and Major Depression: A Review

A Neuroimmunological Model of Schizophrenia and Major Depression: A Review

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