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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 references 197

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          Microglia: a sensor for pathological events in the CNS.

          The most characteristic feature of microglial cells is their rapid activation in response to even minor pathological changes in the CNS. Microglia activation is a key factor in the defence of the neural parenchyma against infectious diseases, inflammation, trauma, ischaemia, brain tumours and neurodegeneration. Microglia activation occurs as a graded response in vivo. The transformation of microglia into potentially cytotoxic cells is under strict control and occurs mainly in response to neuronal or terminal degeneration, or both. Activated microglia are mainly scavenger cells but also perform various other functions in tissue repair and neural regeneration. They form a network of immune alert resident macrophages with a capacity for immune surveillance and control. Activated microglia can destroy invading micro-organisms, remove potentially deleterious debris, promote tissue repair by secreting growth factors and thus facilitate the return to tissue homeostasis. An understanding of intercellular signalling pathways for microglia proliferation and activation could form a rational basis for targeted intervention on glial reactions to injuries in the CNS.
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            Inhibition of  T Cell Proliferation by Macrophage Tryptophan Catabolism

            We have recently shown that expression of the enzyme indoleamine 2,3-dioxygenase (IDO) during murine pregnancy is required to prevent rejection of the allogeneic fetus by maternal T cells. In addition to their role in pregnancy, IDO-expressing cells are widely distributed in primary and secondary lymphoid organs. Here we show that monocytes that have differentiated under the influence of macrophage colony-stimulating factor acquire the ability to suppress T cell proliferation in vitro via rapid and selective degradation of tryptophan by IDO. IDO was induced in macrophages by a synergistic combination of the T cell–derived signals IFN-γ and CD40-ligand. Inhibition of IDO with the 1-methyl analogue of tryptophan prevented macrophage-mediated suppression. Purified T cells activated under tryptophan-deficient conditions were able to synthesize protein, enter the cell cycle, and progress normally through the initial stages of G1, including upregulation of IL-2 receptor and synthesis of IL-2. However, in the absence of tryptophan, cell cycle progression halted at a mid-G1 arrest point. Restoration of tryptophan to arrested cells was not sufficient to allow further cell cycle progression nor was costimulation via CD28. T cells could exit the arrested state only if a second round of T cell receptor signaling was provided in the presence of tryptophan. These data reveal a novel mechanism by which antigen-presenting cells can regulate T cell activation via tryptophan catabolism. We speculate that expression of IDO by certain antigen presenting cells in vivo allows them to suppress unwanted T cell responses.
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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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                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
                3181623
                22034110
                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.

                Categories
                Basic Research

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