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      Cytokines, neurophysiology, neuropsychology, and psychiatric symptoms. Translated title: Citoquinas: neurofisiología, neuropsicología y síntomas psiquiátricos Translated title: Cytokines et symptômes psychiatriques

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          Abstract

          Recent research has overcome the old paradigms of the brain as an immunologically privileged organ, and of the exclusive role of neurotransmitters and neuropeptides as signal transducers in the central nervous system. Growing evidence suggests that the signal proteins of the immune system - the cytokines - are also involved in modulation of behavior and induction of psychiatric symptoms. This article gives an overview on the nature of cytokines and the proposed mechanisms of immune-to-brain interaction. The role of cytokines in psychiatric symptoms, syndromes, and disorders like sickness behavior, major depression, and schizophrenia are discussed together with recent immunogenetic findings.

          Translated abstract

          La investigación reciente ha sobrepasado los antiguos paradigmas que consideraban que el cerebro era un órgano inmunológicamente privilegiado y que los neurotransmisores y neuropéptidos tenían un papel exclusivo en la transducción de señales en el sistema nervioso central. Existe creciente evidencia que sugiere que las proteínas de señales del sistema inmune - las citoquinas - también participan en la modulación de la conducta y en la inducción de síntomas psiquiátricos. Estre artículo entrega una visión panorámica acerca de la naturaleza de las citoquinas y los mecanismos propuestos de la interacción entre la inmunidad y el cerebro. Se discute el papel de las citoquinas en síntomas, síndromes y trastornos psiquiátricos como la conducta de enfermedad, la depresión mayor y la esquizofrenia, como también recientes hallazgos inmunogenéticos.

          Translated abstract

          La recherche récente a dépassé les anciens paradigmes considérant le cerveau comme un organe immunologiquement privilégié et le rôle exclusif des neurotransmetteurs et des neuropeptides comme transducteurs de signaux dans le système nerveux central. De plus en plus d'arguments suggèrent que les protéines de signal du système immunitaire - les cytokines - sont aussi impliquées dans la modulation du comportement et le développement des symptômes psychiatriques. Cet article tente de donner un rapide aperçu de la nature des cytokines et des mécanismes supposés mis en jeu dans l'interaction entre immunité et cerveau. Sont présentés le rôle des cytokines dans les symptômes psychiatriques, syndromes et troubles tels que le «comportement de maladie», la dépression majeure et la schizophrénie ainsi que les découvertes récentes en immunogénétique.

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          Most cited references181

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          IL-27, a heterodimeric cytokine composed of EBI3 and p28 protein, induces proliferation of naive CD4+ T cells.

          An efficient Th1-driven adaptive immune response requires activation of the T cell receptor and secretion of the T cell stimulatory cytokine IL-12 by activated antigen-presenting cells. IL-12 triggers Th1 polarization of naive CD4(+) T cells and secretion of IFN-gamma. We describe a new heterodimeric cytokine termed IL-27 that consists of EBI3, an IL-12p40-related protein, and p28, a newly discovered IL-12p35-related polypeptide. IL-27 is an early product of activated antigen-presenting cells and drives rapid clonal expansion of naive but not memory CD4(+) T cells. It also strongly synergizes with IL-12 to trigger IFN-gamma production of naive CD4(+) T cells. IL-27 mediates its biologic effects through the orphan cytokine receptor WSX-1/TCCR.
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            Control of synaptic strength by glial TNFalpha.

            Activity-dependent modulation of synaptic efficacy in the brain contributes to neural circuit development and experience-dependent plasticity. Although glia are affected by activity and ensheathe synapses, their influence on synaptic strength has largely been ignored. Here, we show that a protein produced by glia, tumor necrosis factor alpha (TNFalpha), enhances synaptic efficacy by increasing surface expression of AMPA receptors. Preventing the actions of endogenous TNFalpha has the opposite effects. Thus, the continual presence of TNFalpha is required for preservation of synaptic strength at excitatory synapses. Through its effects on AMPA receptor trafficking, TNFalpha may play roles in synaptic plasticity and modulating responses to neural injury.
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              Cytokine-induced sickness behaviour: mechanisms and implications.

              Sickness behaviour represents the expression of the adaptive reorganization of the priorities of the host during an infectious episode. This process is triggered by pro-inflammatory cytokines produced by peripheral phagocytic cells in contact with invading micro-organisms. The peripheral immune message is relayed to the brain via a fast neural pathway and a slower humoral pathway, resulting in the expression of pro-inflammatory cytokines in macrophage-like cells and microglia in the brain. The cellular and molecular components of this previously unsuspected system are being progressively identified. These advances are opening new avenues for understanding brain disorders, including depression.
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                Author and article information

                Contributors
                Psychiatric Hospital, Ludwig-Maximilians-University Munich, Munich, Germany
                Journal
                Dialogues Clin Neurosci
                Dialogues Clin Neurosci
                Dialogues in Clinical Neuroscience
                Les Laboratoires Servier (France )
                1294-8322
                1958-5969
                June 2003
                June 2003
                : 5
                : 2
                : 139-153
                Affiliations
                Psychiatric Hospital, Ludwig-Maximilians-University Munich, Munich, Germany
                Author notes
                Article
                10.31887/DCNS.2003.5.2/mschwarz
                3181623
                22034110
                c7309604-3484-4309-ac52-6e33784c7ad0
                Copyright: © 2003 LLS

                This is an open-access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by-nc-nd/3.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Categories
                Basic Research

                Neurosciences
                psychoneuroimmunology,schizophrenia,cytokine,major depression,immunogenetics,sickness behavior

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