Increased Numbers of CD5 B Lymphocytes in Schizophrenic Patients

McAllister, Cathy G.; Rapaport, Mark Hyman; Pickar, David; Podruchny, Teresa A.; Christison, George W.; Alphs, Larry; Paul, Steven M.

doi:10.1001/archpsyc.1989.01810100032006

Cited by 88 publications

(17 citation statements)

References 33 publications

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“…In a number of studies schizophrenic and schizoaffective patients were compiled together in one sample [12-14, 16, 29, 53, 55]. Other studies did not differentiate between acutely and chronically ill patients [17,[56][57][58][59].…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

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: Discussionmentioning

confidence: 99%

“…There are complex interactions between the cellular immunological system and the cytokines. B lymphocytes in medicated patients were reported to be either unchanged [16,29] or elevated ( [58] in 30% of the Table 3 patients) [60]. In unmedicated schizophrenics unchanged [29] as well as elevated [16] numbers were found.…”

Section: Discussionmentioning

confidence: 99%

Immunological Dysfunction in Schizophrenia: A Systematic Approach

Rothermundt¹,

Arolt²,

Weitzsch³

et al. 1998

Neuropsychobiology

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“…In other studies 1711, CDS+B cells do not appear to increase during HIV infection. Unexpectedly, augmented numbers of CDS+B cells have been observed in psychiatric patients [72], alluding to autoimmune mechanisms playing a role in the pathogenesis of schizophrenia. In cancer [73], the frequencies of CD5 + B cells ranged from 14 to 58% in the controls and from 15 to 83% in the patient population.…”

Section: Various Conditionsmentioning

confidence: 99%

Human CD5‐positive B Cells in lymphoid malignancy and connective tissue diseases

Youinou

Mackenzie

Lamour

et al. 1993

Eur J Clin Investigation

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Abstract. The current literature on human CD5-positive B cells (CD5 + B cells) has been analysed, with a special emphasis on non organ-specific auto-immune diseases. Malignant cells of most of the chronic lymphoid leukaemias of the B cell lineage express the CD5 molecule. Antibodies of the IgM class produced by leukaemic B cells are multispecific auto-antibodies. The CD5+B cell subset may be expanded in non organ-specific autoimmune diseases, such as rheumatoid arthritis, primary Sjogren's syndrome, systemic lupus erythematosus. This holds true for various conditions, including organ-specific auto-immune diseases. Since auto-immune features are common in lymphoproliferative disorders, and the latter be a complication in non organ-specific auto-immune diseases, CD5 + B cells may represent an intermediatary between these auto-immune diseases and B cell lymphoproliferations. Studies on the regulation of CDS+B cell production and function are likely to shed light on the aetiology of, and pathogenetic mechanisms operating in the different disease states.

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“…14 This is reminiscent of findings in multiple sclerosis of 'a B-cell response to a specific antigen occurring in the central nervous system, whereas corresponding clones are absent from the peripheral circulation'; 15 (b) elevated soluble interleukin-2 (IL-2) receptors in serum, comparable to elevations in rheumatoid arthritis, systemic lupus erythematosus, and multiple sclerosis -all known or suspected to be autoimmune. Increased levels of IL-2 in CSF, 16 correlating with recurrence of symptoms in schizophrenia; 17 (c) increased interleukin-6 (IL-6) 18 indicative of immune system activation; (d) increased numbers of CD5 þ B lymphocytes, 19 similar to autoimmune diseases including rheumatoid arthritis, progressive systemic sclerosis, Graves' disease, Sjogren's syndrome and IDDM. 20 Many genetic studies in schizophrenia have implicated genes known to determine predisposition to autoimmune diseases especially genes associated with the major histocompatibility complex (MHC).…”

Section: Reported Immunological Abnormalities In Schizophrenia Includementioning

confidence: 99%

Rationale for a trial of immunosuppressive therapy in acute schizophrenia

et al. 2007

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Schizophrenia is a debilitating, costly, socially disruptive, life-threatening disease in which available treatments are largely palliative and empirical, and produce significant short-and long-term side effects. Therefore, a strong case can made for exploring alternative treatments with a rational basis for use in this disease. Considerable evidence indicates that autoimmune processes may be involved in some forms of schizophrenia, including altered risk of certain autoimmune diseases in patients and their relatives, shared epidemiological features, and apparent involvement of genes known to influence the immune response repertoire. Attempts to provide direct evidence for autoimmune processes have proven elusive, possibly due to the technical difficulty inherent in accessing autoantibodies with high affinity for brain cell-surface receptors. In view of this impasse, we argue for a well-designed trial in schizophrenia of immunosuppressive therapy, which is now the mainstay of therapy for many autoimmune diseases. Analysis of disease states in which immunosuppression has been effectively used over many decades provides guidelines necessary for a meaningful trial.

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Increased Numbers of CD5 B Lymphocytes in Schizophrenic Patients

Cited by 88 publications

References 33 publications

Immunological Dysfunction in Schizophrenia: A Systematic Approach

Immunological Dysfunction in Schizophrenia: A Systematic Approach

Human CD5‐positive B Cells in lymphoid malignancy and connective tissue diseases

Rationale for a trial of immunosuppressive therapy in acute schizophrenia

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