Lymphocyte subpopulations in peripheral blood from schizophrenic patients

Yyland, H.; Ness, Aslaug; Lunde, Hanne Marie Bøe

doi:10.1111/j.1600-0447.1980.tb00584.x

Cited by 57 publications

(15 citation statements)

References 13 publications

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“…A role of T cells in schizophrenia though was first indicated more than 35 years ago (Nyland et al 1980), the macrophage-T lymphocyte theory of schizophrenia was proposed in 1992 and this was further supported in 1995 (Smith 1992;Smith and Maes 1995). Subsequent to this, many studies consistently demonstrated aberrant Tcell mediated immunity in schizophrenia (Table 1).…”

Section: T Cell Theory Of Schizophrenia Revisitedmentioning

confidence: 94%

Adaptive Immunity in Schizophrenia: Functional Implications of T Cells in the Etiology, Course and Treatment

Debnath

2015

J Neuroimmune Pharmacol

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Schizophrenia is a severe and highly complex neurodevelopmental disorder with an unknown etiopathology. Recently, immunopathogenesis has emerged as one of the most compelling etiological models of schizophrenia. Over the past few years considerable research has been devoted to the role of innate immune responses in schizophrenia. The findings of such studies have helped to conceptualize schizophrenia as a chronic low-grade inflammatory disorder. Although the contribution of adaptive immune responses has also been emphasized, however, the precise role of T cells in the underlying neurobiological pathways of schizophrenia is yet to be ascertained comprehensively. T cells have the ability to infiltrate brain and mediate neuro-immune cross-talk. Conversely, the central nervous system and the neurotransmitters are capable of regulating the immune system. Neurotransmitter like dopamine, implicated widely in schizophrenia risk and progression can modulate the proliferation, trafficking and functions of T cells. Within brain, T cells activate microglia, induce production of pro-inflammatory cytokines as well as reactive oxygen species and subsequently lead to neuroinflammation. Importantly, such processes contribute to neuronal injury/death and are gradually being implicated as mediators of neuroprogressive changes in schizophrenia. Antipsychotic drugs, commonly used to treat schizophrenia are also known to affect adaptive immune system; interfere with the differentiation and functions of T cells. This understanding suggests a pivotal role of T cells in the etiology, course and treatment of schizophrenia and forms the basis of this review.

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Section: T Cell Theory Of Schizophrenia Revisitedmentioning

confidence: 94%

Adaptive Immunity in Schizophrenia: Functional Implications of T Cells in the Etiology, Course and Treatment

Debnath

2015

J Neuroimmune Pharmacol

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“…= 6.3, range [5][6][7][8][9][10][11][12][13][14][15][16][17][18][19]. In order to rule out the possibility of a schizophreniform disorder, patients in the present study were chosen if they had at least one previous hospitalization.…”

Section: Methods and Subjectsmentioning

confidence: 99%

Changes in Interleukin-1β and Soluble Interleukin-2 Receptor Levels in CSF and Serum of Schizophrenic Patients

Barak¹,

Barak²,

Levine³

et al. 1995

Journal of Basic and Clinical Physiology and Pharmacology

102

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Some evidence points towards a possible autoimmune role in the aetiology of schizophrenia. Experimental findings provide contradictory results regarding abnormalities in cytokine production in this disorder. In the present study we tested the production of cytokines in CSF and serum in 16 schizophrenic patients and 10 healthy controls (tumor necrosis factor alpha - TNF alpha; interleukins IL-1 beta, IL-2, IL-6, soluble IL-2 receptor). Cytokine levels were evaluated by radioactively-labeled antibodies (IL-1 beta, IL-2, IL-6), by enzyme-linked immunoassay (TNF) and by a sandwich enzyme immunoassay (soluble IL-2 receptor). No significant differences were found in either CSF fluid or serum levels of TNF and IL-2 or IL-6. Interleukin-1 beta was significantly decreased in patients' CSF and serum as compared to controls. Soluble interleukin-2 receptor levels were decreased in CSF of patients, but highly increased in their serum in comparison with controls. Changes in various cytokine levels in CSF fluid and serum of schizophrenic patients probably reflect interrelated process of growth, degeneration or neuroimmunological abnormalities, which may all play a role in the pathophysiology of schizophrenia. The present study supports evidence for change in immune activation, probably of peripheral origin, in schizophrenic patients.

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“…On the cellular level, a decrease in the reactivity of lymphocytes [47][48] and the presence of large morphologically abnormal lymphocytes [47] were reported. A decrease in the percentage of T cells in schizophrenic patients with a severe recurrence was also observed [49] , whereas in untreated patients an increase in T suppressor lymphocytes was noted [50] . In addition, an increase in the ratio of T helper cells to T suppressor cells was found to correlate with the patients' psychiatric condition [51] .…”

Section: Discussionmentioning

confidence: 99%

Blind Verification of Elevated Platelet Autoantibodies in Serum of Schizophrenic Patients – Part II: Adult Subjects

Spivak¹,

Schechtman

Schönherz-Pine³

et al. 2009

Neuropsychobiology

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Background: In our preceding study, we assayed in a blind fashion the blood sera of young normal subjects and schizophrenic patients for levels of platelet autoantibodies (PAA). The recorded PAA titers of the schizophrenic patients were significantly higher than those of the normal subjects. This observation has lent support to this test being used as an objective evaluation of schizophrenia in young subjects in the future. In addition, this finding strongly suggested that the etiology of a distinct group of sufferers of this disorder could have originated from an autoimmune reaction against platelets which can, under certain conditions, cross-react with brain tissue. Aims: In the present study, PAA titers in the sera of adult schizophrenic patients and matched normal subjects were determined analogously to the preceding study. The effect of hospitalization and drug treatments on the apparent blood test scoring in adult subjects could thus be evaluated. Methods: A total of 46 schizophrenia patients (30 men and 16 women) aged 19–45 years (mean ± SD: 31.7 ± 8.0 years) with a minimum score of 60 on the Positive and Negative Symptom Scale and 43 healthy control subjects (22 men and 21 women) aged 21–44 years (mean ± SD: 31.9 ± 6.9 years) participated in the study. The blood titers of PAA were evaluated in a single-blind fashion using an optimized ELISA test scored by optical density (OD) units. A positive test was defined as a value above 1.3 OD units. Results: The titers of PAA in the group of schizophrenic patients (1.1 ± 0.55 OD units, range: 0.360–2.285 OD units) were significantly higher in comparison to those of the healthy control subjects (0.81 ± 0.37 OD units, range: 0.360–1.704 OD units; p = 0.004, two-tailed unpaired t-test). Significantly more schizophrenic patients showed a positive test (15 patients out of 46) than the control subjects (5 out of 43). However, significantly higher OD values of 1.55 ± 0.5 were recorded in the group of patients with less than 3 years of registered disease (n = 16, age 19–30 years), while in the group with 4–20 years of hospitalization (n = 30, age 24–45 years) the recorded OD values (0.85 ± 0.4 OD units) were practically indistinguishable from those of the control group. Conclusions: In the adult schizophrenic patients, the PAA blood test remains valid for patients who were hospitalized for less than 3 years. Drug treatment, length of disease and age can be assumed to reduce the PAA level considerably.

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Lymphocyte subpopulations in peripheral blood from schizophrenic patients

Cited by 57 publications

References 13 publications

Adaptive Immunity in Schizophrenia: Functional Implications of T Cells in the Etiology, Course and Treatment

Adaptive Immunity in Schizophrenia: Functional Implications of T Cells in the Etiology, Course and Treatment

Changes in Interleukin-1β and Soluble Interleukin-2 Receptor Levels in CSF and Serum of Schizophrenic Patients

Blind Verification of Elevated Platelet Autoantibodies in Serum of Schizophrenic Patients – Part II: Adult Subjects

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