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<OAI-PMH schemaLocation=http://www.openarchives.org/OAI/2.0/ http://www.openarchives.org/OAI/2.0/OAI-PMH.xsd> <responseDate>2018-01-15T18:24:20Z</responseDate> <request identifier=oai:HAL:hal-01295637v1 verb=GetRecord metadataPrefix=oai_dc>http://api.archives-ouvertes.fr/oai/hal/</request> <GetRecord> <record> <header> <identifier>oai:HAL:hal-01295637v1</identifier> <datestamp>2017-12-21</datestamp> <setSpec>type:ART</setSpec> <setSpec>subject:sdv</setSpec> <setSpec>collection:UNIV-RENNES1</setSpec> <setSpec>collection:UNIV-AG</setSpec> <setSpec>collection:IRSET</setSpec> <setSpec>collection:IRSET-HIAEC</setSpec> <setSpec>collection:IFR140</setSpec> <setSpec>collection:BIOSIT</setSpec> <setSpec>collection:UR1-UFR-SVE</setSpec> <setSpec>collection:STATS-UR1</setSpec> <setSpec>collection:UR1-HAL</setSpec> <setSpec>collection:EHESP</setSpec> <setSpec>collection:USPC</setSpec> <setSpec>collection:UR1-SDV</setSpec> <setSpec>collection:IRSET-2</setSpec> <setSpec>collection:UNIV-ANGERS</setSpec> </header> <metadata><dc> <publisher>HAL CCSD</publisher> <title lang=en>Potential Therapeutic Aspects of Alarmin Cytokine Interleukin 33 or Its Inhibitors in Various Diseases</title> <creator>Imran Arshad, Muhammad</creator> <creator>Ahmad Khan, Hilal</creator> <creator>Noel, Gregory</creator> <creator>Piquet-Pellorce, Claire</creator> <creator>Samson, Michel</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> <description>International audience</description> <source>ISSN: 0149-2918</source> <source>Clinical Therapeutics</source> <publisher>Elsevier</publisher> <identifier>hal-01295637</identifier> <identifier>https://hal-univ-rennes1.archives-ouvertes.fr/hal-01295637</identifier> <source>https://hal-univ-rennes1.archives-ouvertes.fr/hal-01295637</source> <source>Clinical Therapeutics, Elsevier, 2016, 38 (5), pp.1000-1016. 〈10.1016/j.clinthera.2016.02.021〉</source> <identifier>PUBMED : 26992663</identifier> <relation>info:eu-repo/semantics/altIdentifier/pmid/26992663</relation> <identifier>DOI : 10.1016/j.clinthera.2016.02.021</identifier> <relation>info:eu-repo/semantics/altIdentifier/doi/10.1016/j.clinthera.2016.02.021</relation> <language>en</language> <subject lang=en> therapeutic aspects</subject> <subject lang=en> Immunity</subject> <subject lang=en>diseases</subject> <subject lang=en> IL-33</subject> <subject>[SDV] Life Sciences [q-bio]</subject> <type>info:eu-repo/semantics/article</type> <type>Journal articles</type> <description lang=en>Purpose The purpose of this review was to examine the comprehensively accumulated data regarding potential therapeutic aspects of exogenous administration of interleukin 33 (IL-33) or its antagonists in allergic, cancerous, infectious, and inflammatory diseases. Methods A selected review was undertaken of publications that examined the protective and exacerbating effects of IL-33 or its inhibitors in different diseases. Mechanisms of action are summarized to examine the putative role of IL-33 in various diseases. Findings IL-33 promoted antibacterial, antiviral, anti-inflammatory, and vaccine adjuvant functions. However, in TH2-biased respiratory, allergic, parasitic, and inflammatory conditions, IL-33 exhibited disease-sensitizing effects. The alarmin cytokine IL-33 induced protective effects in diseases via recruitment of regulatory T cells; antiviral CD8+ cells, natural killer cells, γδ T cells, and nuocytes; antibacterial and antifungal neutrophils or macrophages; vaccine-associated B/T cells; and inhibition of nuclear factor–κB–mediated gene transcription. In contrast, IL-33 exacerbated the disease process by increasing TH2 cytokines, IgE and eosinophilic immune responses, and inhibition of leukocyte recruitment in various diseases. Implications The protective or exacerbated aspects of use of IL-33 or its inhibitors are dependent on the type of infection or inflammatory condition, duration of disease (acute or chronic), organ involved, cytokine microenvironment, dose or kinetics of IL-33, and genetic predisposition. The alarmin cytokine IL-33 acts at cellular, molecular, and transcriptional levels to mediate pluripotent functions in various diseases and has potential therapeutic value to mitigate the disease process</description> <date>2016</date> </dc> </metadata> </record> </GetRecord> </OAI-PMH>