T-lymphocyte subpopulations in schizophrenic patients

Henneberg, A.E.; Riedl, B.; Dumke, Hans O.; Kornhuber, H. H.

doi:10.1007/bf01735051

Cited by 53 publications

(8 citation statements)

References 13 publications

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“…Nyland et al [10] showed a decreased number of T lymphocytes in acute but not in chronic schizophrenics. An elevated number of T cells was reported by two groups [11][12][13][14] while others (including ours) demonstrated no change in T cell number [15][16][17][18][19][20]. Inhomogenuous results have been reported concerning several T lymphocyte subtypes, B lymphocytes and natural killer cells (NK cells).…”

Section: Introductionmentioning

confidence: 70%

“…CD-4-positive T helper cells were found to be increased in unmedicated schizophrenics [11][12][13], but there are inconsistencies regarding those results even within the same studies. Müller et al [14] in 1993 reproduced their 1991 findings with respect to the absolute CD-4-positive cell number but not regarding the relative number.…”

Section: Discussionmentioning

confidence: 99%

“…Henneberg et al [11] observed a tendency towards an increased T suppressor cell number, Masserini et al [16] demonstrated unchanged CD-8-positive cell numbers in medicated schizophrenic patients but increased numbers in drug-free patients while Ackenheil et al [12] observed a higher number in medicated schizophrenics.…”

Section: Discussionmentioning

confidence: 99%

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Immunological Dysfunction in Schizophrenia: A Systematic Approach

Rothermundt¹,

Arolt²,

Weitzsch³

et al. 1998

Neuropsychobiology

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Background: In the present study, immunological alterations were investigated as one possible factor contributing towards the pathogenesis of schizophrenia. Specifically cellular changes, deviating cytokine production and interfering variables were studied in order to improve our understanding of how these factors interact. Method: 44 acutely ill schizophrenics were compared with matched healthy controls. Cell numbers were determined by flow cytometry and cytokine production by whole blood assay and ELISA. A criss-cross technique was employed for the assessment of interfering serum factors. Results: Cell counts for leukocytes, lymphocytes, pan T cells, activated T cells and the absolute B cell count of the schizophrenic patients were all within normal limits. The absolute and relative monocyte counts, the number of IL-2 receptor carrying T cells and the relative B cell count were slightly elevated. IL-2 and IFN-γ production were increased while IL-10 production, the sIL-2R and cortisol levels remained unchanged. No interfering serum factors were detected. Conclusion: The deficient production of TH-1 cytokines in schizophrenia is not due either to a changed number of immunocompetent cells or to a counterregulation of the TH-2 cytokine IL-10. Serum factors in in vitro testing are not responsible for the deficient cytokine production.

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Section: Introductionmentioning

confidence: 70%

Section: Discussionmentioning

confidence: 99%

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Immunological Dysfunction in Schizophrenia: A Systematic Approach

Rothermundt¹,

Arolt²,

Weitzsch³

et al. 1998

Neuropsychobiology

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“…5 Henneberg et al 1990 Acute schizophrenia patients (n=30) Significant increases in the number of T cells. 6 Masserini et al 1990 Schizophrenia and schizophrenia spectrum disorders (n=42)…”

Section: T Cell Theory Of Schizophrenia Revisitedmentioning

confidence: 99%

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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“…It is difficult, however, to inter pret these findings, because all of the patients were receiv ing neuroleptic treatment during the study. Henneberg et al [28] found a significant increase in the numbers of Pan T and T helper cells in acute schizophrenic patients (phar macologically treated). In a recent study, Achiron et al [29] evaluated T cell subsets in psychotic, drug-free, acute schizophrenic patients.…”

Section: T Cell Changesmentioning

confidence: 99%

Schizophrenia and Autoimmunity – A Possible Etiological Mechanism?

1994

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Schizophrenia is a chronic disease which begins during early adulthood and persists throughout life. It may appear in two main clinical patterns: chronic progressive and relapsing-remitting. The diagnosis is based entirely on clinical data, as no auxiliary laboratory tests are available. Schizophrenia has a heterogeneous clinical expression which may reflect different etiological factors, such as genetic susceptibility, dysfunction of different neurotransmitter systems or environmental, stressogenic and interfamilial influences. Recently, an autoimmune hypothesis has gained acceptance, which proposes that schizophrenia is one of a spectrum of neuropsychiatric diseases in which an autoimmune attack on the brain occurs. It is also possible, however, that the immunological changes seen in schizophrenic patients are secondary to the disease itself. The main evidence supporting an autoimmune hypothesis is the presence of immunological alterations in schizophrenia that also occur in other autoimmune diseases, e.g. an elevation in serum immunoglobulin levels, a decrease in mitogen responses, morphologically abnormal lymphocytes, an increase in antibrain antibodies, an increase in antibodies to nuclear factor, and a decrease in CD4+ T cells. An autoimmune etiology, if proven correct in the pathogenesis of schizophrenia, would have potential implications for the direction of future psychopharmacological therapies.

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T-lymphocyte subpopulations in schizophrenic patients

Cited by 53 publications

References 13 publications

Immunological Dysfunction in Schizophrenia: A Systematic Approach

Immunological Dysfunction in Schizophrenia: A Systematic Approach

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

Schizophrenia and Autoimmunity – A Possible Etiological Mechanism?

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