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<title lang=en>The aryl hydrocarbon receptor is functionally upregulated early in the course of human T-cell activation</title>
<creator>Prigent, Laurie</creator>
<creator>Robineau, Marc</creator>
<creator>Jouneau, Stéphane</creator>
<creator>Morzadec, Claudie</creator>
<creator>Louarn, Laetitia</creator>
<creator>Vernhet, Laurent</creator>
<creator>Fardel, Olivier</creator>
<creator>Sparfel, Lydie</creator>
<contributor>Institut de recherche, santé, environnement et travail [Rennes] (Irset) ; Université d'Angers (UA) - Université des Antilles et de la Guyane (UAG) - Université de Rennes 1 (UR1) - École des Hautes Études en Santé Publique [EHESP] (EHESP) - Institut National de la Santé et de la Recherche Médicale (INSERM) - Structure Fédérative de Recherche en Biologie et Santé de Rennes ( Biosit : Biologie - Santé - Innovation Technologique )</contributor>
<contributor>Contaminants Chimiques, immunité et Inflammation ; Institut de recherche, santé, environnement et travail [Rennes] (Irset) ; Université d'Angers (UA) - Université des Antilles et de la Guyane (UAG) - Université de Rennes 1 (UR1) - École des Hautes Études en Santé Publique [EHESP] (EHESP) - Institut National de la Santé et de la Recherche Médicale (INSERM) - Structure Fédérative de Recherche en Biologie et Santé de Rennes ( Biosit : Biologie - Santé - Innovation Technologique ) - Université d'Angers (UA) - Université des Antilles et de la Guyane (UAG) - Université de Rennes 1 (UR1) - École des Hautes Études en Santé Publique [EHESP] (EHESP) - Institut National de la Santé et de la Recherche Médicale (INSERM) - Structure Fédérative de Recherche en Biologie et Santé de Rennes ( Biosit : Biologie - Santé - Innovation Technologique )</contributor>
<description>International audience</description>
<source>ISSN: 0014-2980</source>
<source>EISSN: 1521-4141</source>
<source>European Journal of Immunology</source>
<publisher>Wiley-VCH Verlag</publisher>
<identifier>hal-01063944</identifier>
<identifier>https://hal.archives-ouvertes.fr/hal-01063944</identifier>
<source>https://hal.archives-ouvertes.fr/hal-01063944</source>
<source>European Journal of Immunology, Wiley-VCH Verlag, 2014, 44 (5), pp.1330--1340. 〈10.1002/eji.201343920〉</source>
<identifier>DOI : 10.1002/eji.201343920</identifier>
<relation>info:eu-repo/semantics/altIdentifier/doi/10.1002/eji.201343920</relation>
<identifier>PUBMED : 24549985</identifier>
<relation>info:eu-repo/semantics/altIdentifier/pmid/24549985</relation>
<language>en</language>
<subject lang=en>Aryl Hydrocarbon</subject>
<subject lang=en>Receptors</subject>
<subject lang=en>Protein Biosynthesis</subject>
<subject lang=en>Active Transport</subject>
<subject lang=en>Cell Nucleus</subject>
<subject lang=en>Aryl Hydrocarbon Hydroxylases</subject>
<subject lang=en>Cytochrome P-450 CYP1A1</subject>
<subject lang=en>Gene Knockdown Techniques</subject>
<subject lang=en>Humans</subject>
<subject lang=en>Interleukins</subject>
<subject lang=en>Lymphocyte Activation</subject>
<subject lang=en>RNA</subject>
<subject lang=en>Messenger</subject>
<subject lang=en>T-Lymphocytes</subject>
<subject lang=en>Up-Regulation</subject>
<subject>[SDV] Life Sciences [q-bio]</subject>
<type>info:eu-repo/semantics/article</type>
<type>Journal articles</type>
<description lang=en>The aryl hydrocarbon receptor (AhR) is a ligand-dependent transcription factor that mediates immunosuppression caused by a variety of environmental contaminants, such as polycyclic aromatic hydrocarbons or dioxins. Recent evidence suggests that AhR plays an important role in T-cell-mediated immune responses by affecting the polarization and differentiation of activated T cells. However, the regulation of AhR expression in activated T cells remains poorly characterized. In the present study, we used purified human T cells stimulated with anti-CD3 and anti-CD28 Abs to investigate the effect of T-cell activation on AhR mRNA and protein expression. The expression of AhR mRNA increased significantly and rapidly after T-cell activation, identifying AhR as an immediate-early activation gene. AhR upregulation occurred in all of the T-cell subtypes, and is associated with its nuclear translocation and induction of the cytochromes P-450 1A1 and 1B1 mRNA expression in the absence of exogenous signals. In addition, the use of an AhR antagonist or siRNA-mediated AhR knockdown significantly inhibited IL-22 expression, suggesting that expression and functional activation of AhR is necessary for the secretion of IL-22 by activated T cells. In conclusion, our data support the idea that AhR is a major player in T-cell physiology.</description>
<date>2014</date>
</dc>
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