The Dopaminergic System in Autoimmune Diseases
Identifieur interne : 000933 ( Pmc/Curation ); précédent : 000932; suivant : 000934The Dopaminergic System in Autoimmune Diseases
Auteurs : Rodrigo Pacheco [Chili] ; Francisco Contreras [Chili] ; Moncef Zouali [France]Source :
- Frontiers in Immunology [ 1664-3224 ] ; 2014.
Abstract
Bidirectional interactions between the immune and the nervous systems are of considerable interest both for deciphering their functioning and for designing novel therapeutic strategies. The past decade has brought a burst of insights into the molecular mechanisms involved in neuroimmune communications mediated by dopamine. Studies of dendritic cells (DCs) revealed that they express the whole machinery to synthesize and store dopamine, which may act in an autocrine manner to stimulate dopamine receptors (DARs). Depending on specific DARs stimulated on DCs and T cells, dopamine may differentially favor CD4+ T cell differentiation into Th1 or Th17 inflammatory cells. Regulatory T cells can also release high amounts of dopamine that acts in an autocrine DAR-mediated manner to inhibit their suppressive activity. These dopaminergic regulations could represent a driving force during autoimmunity. Indeed, dopamine levels are altered in the brain of mouse models of multiple sclerosis (MS) and lupus, and in inflamed tissues of patients with inflammatory bowel diseases or rheumatoid arthritis (RA). The distorted expression of DARs in peripheral lymphocytes of lupus and MS patients also supports the importance of dopaminergic regulations in autoimmunity. Moreover, dopamine analogs had beneficial therapeutic effects in animal models, and in patients with lupus or RA. We propose models that may underlie key roles of dopamine and its receptors in autoimmune diseases.
Url:
DOI: 10.3389/fimmu.2014.00117
PubMed: 24711809
PubMed Central: 3968755
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<front><div type="abstract" xml:lang="en"><p>Bidirectional interactions between the immune and the nervous systems are of considerable interest both for deciphering their functioning and for designing novel therapeutic strategies. The past decade has brought a burst of insights into the molecular mechanisms involved in neuroimmune communications mediated by dopamine. Studies of dendritic cells (DCs) revealed that they express the whole machinery to synthesize and store dopamine, which may act in an autocrine manner to stimulate dopamine receptors (DARs). Depending on specific DARs stimulated on DCs and T cells, dopamine may differentially favor CD4<sup>+</sup>
T cell differentiation into Th1 or Th17 inflammatory cells. Regulatory T cells can also release high amounts of dopamine that acts in an autocrine DAR-mediated manner to inhibit their suppressive activity. These dopaminergic regulations could represent a driving force during autoimmunity. Indeed, dopamine levels are altered in the brain of mouse models of multiple sclerosis (MS) and lupus, and in inflamed tissues of patients with inflammatory bowel diseases or rheumatoid arthritis (RA). The distorted expression of DARs in peripheral lymphocytes of lupus and MS patients also supports the importance of dopaminergic regulations in autoimmunity. Moreover, dopamine analogs had beneficial therapeutic effects in animal models, and in patients with lupus or RA. We propose models that may underlie key roles of dopamine and its receptors in autoimmune diseases.</p>
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<pmc article-type="review-article"><pmc-dir>properties open_access</pmc-dir>
<front><journal-meta><journal-id journal-id-type="nlm-ta">Front Immunol</journal-id>
<journal-id journal-id-type="iso-abbrev">Front Immunol</journal-id>
<journal-id journal-id-type="publisher-id">Front. Immunol.</journal-id>
<journal-title-group><journal-title>Frontiers in Immunology</journal-title>
</journal-title-group>
<issn pub-type="epub">1664-3224</issn>
<publisher><publisher-name>Frontiers Media S.A.</publisher-name>
</publisher>
</journal-meta>
<article-meta><article-id pub-id-type="pmid">24711809</article-id>
<article-id pub-id-type="pmc">3968755</article-id>
<article-id pub-id-type="doi">10.3389/fimmu.2014.00117</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Immunology</subject>
<subj-group><subject>Review Article</subject>
</subj-group>
</subj-group>
</article-categories>
<title-group><article-title>The Dopaminergic System in Autoimmune Diseases</article-title>
</title-group>
<contrib-group><contrib contrib-type="author"><name><surname>Pacheco</surname>
<given-names>Rodrigo</given-names>
</name>
<xref ref-type="aff" rid="aff1"><sup>1</sup>
</xref>
<xref ref-type="aff" rid="aff2"><sup>2</sup>
</xref>
<uri xlink:type="simple" xlink:href="http://frontiersin.org/people/u/98095"></uri>
</contrib>
<contrib contrib-type="author"><name><surname>Contreras</surname>
<given-names>Francisco</given-names>
</name>
<xref ref-type="aff" rid="aff1"><sup>1</sup>
</xref>
<xref ref-type="aff" rid="aff3"><sup>3</sup>
</xref>
<uri xlink:type="simple" xlink:href="http://frontiersin.org/people/u/137318"></uri>
</contrib>
<contrib contrib-type="author"><name><surname>Zouali</surname>
<given-names>Moncef</given-names>
</name>
<xref ref-type="aff" rid="aff4"><sup>4</sup>
</xref>
<xref ref-type="aff" rid="aff5"><sup>5</sup>
</xref>
<xref ref-type="corresp" rid="cor1">*</xref>
<uri xlink:type="simple" xlink:href="http://frontiersin.org/people/u/25082"></uri>
</contrib>
</contrib-group>
<aff id="aff1"><sup>1</sup>
<institution>Laboratory of Neuroimmunology, Fundación Ciencia & Vida</institution>
,<addr-line>Santiago</addr-line>
,<country>Chile</country>
</aff>
<aff id="aff2"><sup>2</sup>
<institution>Programa de Biomedicina, Universidad San Sebastián</institution>
,<addr-line>Santiago</addr-line>
,<country>Chile</country>
</aff>
<aff id="aff3"><sup>3</sup>
<institution>Universidad Andrés Bello, Facultad de Ciencias Biológicas</institution>
,<addr-line>Santiago</addr-line>
,<country>Chile</country>
</aff>
<aff id="aff4"><sup>4</sup>
<institution>INSERM UMR 1132</institution>
,<addr-line>Paris</addr-line>
,<country>France</country>
</aff>
<aff id="aff5"><sup>5</sup>
<institution>University Paris Diderot</institution>
,<addr-line>Paris</addr-line>
,<country>France</country>
</aff>
<author-notes><fn fn-type="edited-by"><p>Edited by: Kendall A. Smith, Weill Medical College of Cornell University, USA</p>
</fn>
<fn fn-type="edited-by"><p>Reviewed by: Kai Fang, University of California Los Angeles, USA; Marco Cosentino, University of Insubria, Italy</p>
</fn>
<corresp content-type="corresp" id="cor1">*Correspondence: Moncef Zouali, INSERM U1132, Centre Viggo Petersen, Hôpital Lariboisière, 2, Rue Ambroise Paré, 75475 Paris Cedex 10, France e-mail: <email>moncef.zouali@wanadoo.fr</email>
</corresp>
<fn fn-type="other" id="fn001"><p>This article was submitted to Inflammation, a section of the journal Frontiers in Immunology.</p>
</fn>
</author-notes>
<pub-date pub-type="epreprint"><day>09</day>
<month>2</month>
<year>2014</year>
</pub-date>
<pub-date pub-type="epub"><day>21</day>
<month>3</month>
<year>2014</year>
</pub-date>
<pub-date pub-type="collection"><year>2014</year>
</pub-date>
<volume>5</volume>
<elocation-id>117</elocation-id>
<history><date date-type="received"><day>19</day>
<month>12</month>
<year>2013</year>
</date>
<date date-type="accepted"><day>05</day>
<month>3</month>
<year>2014</year>
</date>
</history>
<permissions><copyright-statement>Copyright © 2014 Pacheco, Contreras and Zouali.</copyright-statement>
<copyright-year>2014</copyright-year>
<license license-type="open-access" xlink:href="http://creativecommons.org/licenses/by/3.0/"><license-p>This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.</license-p>
</license>
</permissions>
<abstract><p>Bidirectional interactions between the immune and the nervous systems are of considerable interest both for deciphering their functioning and for designing novel therapeutic strategies. The past decade has brought a burst of insights into the molecular mechanisms involved in neuroimmune communications mediated by dopamine. Studies of dendritic cells (DCs) revealed that they express the whole machinery to synthesize and store dopamine, which may act in an autocrine manner to stimulate dopamine receptors (DARs). Depending on specific DARs stimulated on DCs and T cells, dopamine may differentially favor CD4<sup>+</sup>
T cell differentiation into Th1 or Th17 inflammatory cells. Regulatory T cells can also release high amounts of dopamine that acts in an autocrine DAR-mediated manner to inhibit their suppressive activity. These dopaminergic regulations could represent a driving force during autoimmunity. Indeed, dopamine levels are altered in the brain of mouse models of multiple sclerosis (MS) and lupus, and in inflamed tissues of patients with inflammatory bowel diseases or rheumatoid arthritis (RA). The distorted expression of DARs in peripheral lymphocytes of lupus and MS patients also supports the importance of dopaminergic regulations in autoimmunity. Moreover, dopamine analogs had beneficial therapeutic effects in animal models, and in patients with lupus or RA. We propose models that may underlie key roles of dopamine and its receptors in autoimmune diseases.</p>
</abstract>
<kwd-group><kwd>dendritic cell</kwd>
<kwd>regulatory T cell</kwd>
<kwd>Th17</kwd>
<kwd>Crohn’s disease</kwd>
<kwd>multiple sclerosis</kwd>
<kwd>ulcerative colitis</kwd>
<kwd>systemic lupus erythematosus</kwd>
<kwd>rheumatoid arthritis</kwd>
</kwd-group>
<counts><fig-count count="3"></fig-count>
<table-count count="1"></table-count>
<equation-count count="0"></equation-count>
<ref-count count="126"></ref-count>
<page-count count="17"></page-count>
<word-count count="14838"></word-count>
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</article-meta>
</front>
</pmc>
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