Aberrant T cell-mediated immunity in untreated schizophrenic patients: Deficient interleukin-2 production

INSERM U25, Hôpital Necker, Paris, France.
American Journal of Psychiatry (Impact Factor: 12.3). 06/1989; 146(5):609-16. DOI: 10.1176/ajp.146.5.609
Source: PubMed


The authors examined the immune status at the cellular and humoral levels of 16 untreated schizophrenic patients. No abnormality in the distribution of T cell subsets (CD4+, CD8+) was detected. The proliferative response to the T cell mitogen phytohemagglutinin was normal. No increase in the number of T cells showing activation markers, such as human leukocyte antigens and interleukin-2 receptors, was noted. Conversely, function studies revealed a clear deficiency in interleukin-2 production by purified T cells. This lower production was probably intrinsic to the patients' T cells, since interleukin-2 production showed normal sensitivity to prostaglandin E2-mediated down-regulation by autologous monocytes.

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    ABSTRACT: Growing evidence suggests that the immune, endocrine, and nervous systems interact with each other through cytokines, hormones, and neurotransmitters. The activation of the cytokine systems may be involved in the neuropathological changes occurring in the central nervous system (CNS) of schizophrenic patients. Numerous studies report that treatment with antipsychotic drugs affects the cytokine network. Hence, it is plausible that the influence of antipsychotics on the cytokine systems may be responsible for their clinical efficacy in schizophrenia. This article reviews current data on the cytokine-modulating potential of antipsychotic drugs. First, basic information on the cytokine networks with special reference to their role in the CNS as well as an up-to-date knowledge of the cytokine alterations in schizophrenia is outlined. Second, the hitherto published studies on the influence of antipsychotics on the cytokine system are reviewed. Third, the possible mechanisms underlying antipsychotics' potential to influence the cytokine networks and the most relevant aspects of this activity are discussed. Finally, limitations of the presented studies and prospects of future research are delineated.
    Brain Behavior and Immunity 12/2006; 20(6):532-45. DOI:10.1016/j.bbi.2006.02.002 · 5.89 Impact Factor
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    • "In contrast, the specific, ''adaptive'' immune system appears to be imbalanced in schizophrenia. There is a decreased in vitro production of IL-2 (Bessler et al., 1995; Cazzullo et al., 1998; Ganguli et al., 1989, 1995; Villemain et al., 1989; Zhang et al., 2002a), as well as a decreased production of interferon-(Arolt et al., 2000; Rothermund et al., 1998; Wilke et al., 1996). Both findings suggested that the Th-1 system is underactivated in schizophrenia. "
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    ABSTRACT: Although the potential key role that lipids may have in schizophrenia is not fully understood, multiple lines of evidence to date implicate the lipid environment in the behavior of neurotransmitter systems. Decreased phospholipid polyunsaturated fatty acids (PUFAs) have been demonstrated in both brain and peripheral membranes in schizophrenia, which is consistent with the hypothesis of myelin-related dysfunction in schizophrenia. Membrane defects, such as those induced by decreased PUFAs in phospholipids, can significantly alter a broad range of membrane functions and ipso facto behavior through multiple "downstream" effects. A number of putative mechanisms have been identified to explain the decreased PUFAs in schizophrenia, notably the increased turnover of phospholipids and decreased incorporation of arachidonic acid (AA) in membranes. In addition to increased oxidative stress, altered immune function may also be responsible for increased phospholipase activities. This association is particularly relevant in relation to phospholipids/PUFA, as AA can be converted to a variety of biologically active compounds, such as eicosanoids, which serve as potent messengers in regulating the inflammatory response, as well as endocannabinoids, which may affect schizophrenic psychopathology. Direct evidence of immune changes in some patients with schizophrenia have come to light, particularly in the activities of several cytokines known to be altered in autoimmune dysfunction. Given the diverse physiological function of AA, the specific behavioral symptomatology of schizophrenia is related mostly to the effect of AA changes that regulates neurodevelopment, neurotransmitter homeostasis, phosphatidylinositol signaling, and neuromodulatory actions of endocannabinoids in schizophrenia. Hence, in the current conceptualization, AA may be at a nexus point in the cascade leading to the syndrome of schizophrenia and represents a common biochemical pathway leading to the varied symptomatology of this disorder.
    International Review of Neurobiology 02/2004; 59:297-326. DOI:10.1016/S0074-7742(04)59012-8 · 1.92 Impact Factor
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    • "The key characteristics of the type-1 immune system are the production of IFN-g, IL-2, and IL-12. One of the often replicated findings in schizophrenia is the decreased in vitro production of IL-2 (Villemain et al., 1989; Ganguli et al., 1995; Hornberg et al., 1995; Bessler et al., 1995; Cazzullo et al., 1998). This phenomenon has often been interpreted as the consequence of an exhaustion of the lymphocytes after overproduction of IL-2. "

    Advances in Molecular and Cell Biology 01/2003; 31:999-1031. DOI:10.1016/S1569-2558(03)31045-8
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