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      <source-app name="Horizon">Horizon</source-app>
      <rec-number>1</rec-number>
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      <ref-type name="Journal Article">17</ref-type>
      <work-type>ACLN : Articles dans des revues avec comité de lecture non répertoriées par l'AERES</work-type>
      <contributors>
        <authors>
          <author>
            <style face="bold" font="default" size="100%">Fievet, Nadine</style>
          </author>
          <author>
            <style face="normal" font="default" size="100%">Moussa, M.</style>
          </author>
          <author>
            <style face="normal" font="default" size="100%">Tami, G.</style>
          </author>
          <author>
            <style face="normal" font="default" size="100%">Maubert, B.</style>
          </author>
          <author>
            <style face="bold" font="default" size="100%">Cot, Michel</style>
          </author>
          <author>
            <style face="normal" font="default" size="100%">Deloron, P.</style>
          </author>
          <author>
            <style face="normal" font="default" size="100%">Chaouat, G.</style>
          </author>
        </authors>
      </contributors>
      <titles>
        <title>Plasmodium falciparum induces a Th1/Th2 disequilibrium, favoring the Th1-type pathway, in the human placenta</title>
        <secondary-title>Journal of Infectious Diseases</secondary-title>
      </titles>
      <pages>1530-1534</pages>
      <keywords>
        <keyword>PALUDISME</keyword>
        <keyword>AGENT PATHOGENE</keyword>
        <keyword>FEMME</keyword>
        <keyword>GROSSESSE</keyword>
        <keyword>IMMUNITE</keyword>
        <keyword>IMMUNOLOGIE</keyword>
        <keyword>CELLULE</keyword>
        <keyword>CULTURE IN VITRO</keyword>
        <keyword>ETUDE EXPERIMENTALE</keyword>
        <keyword>TRANSMISSION PLACENTAIRE</keyword>
        <keyword>TH1 CYTOKINE</keyword>
        <keyword>TH2 CYTOKINE</keyword>
        <keyword>CAMEROUN</keyword>
        <keyword>YAOUNDE</keyword>
        <keyword>NKOLDONGO</keyword>
        <keyword>DJOUNGOLO</keyword>
      </keywords>
      <dates>
        <year>2001</year>
      </dates>
      <call-num>fdi:010025993</call-num>
      <language>ENG</language>
      <periodical>
        <full-title>Journal of Infectious Diseases</full-title>
      </periodical>
      <isbn>0002-1899</isbn>
      <number>10</number>
      <electronic-resource-num>10.1086/320201</electronic-resource-num>
      <urls>
        <related-urls>
          <url>https://www.documentation.ird.fr/hor/fdi:010025993</url>
        </related-urls>
        <pdf-urls>
          <url>https://horizon.documentation.ird.fr/exl-doc/pleins_textes/pleins_textes_7/b_fdi_59-60/010025993.pdf</url>
        </pdf-urls>
      </urls>
      <volume>183</volume>
      <remote-database-provider>Horizon (IRD)</remote-database-provider>
      <abstract>During pregnancy, a local and systemic Th2 bias of maternal immunity favors Th1-dependent infections such as malaria. This study measured cytokines secreted in cultures of chorionic villi, placental blood cells (PBC), and serum in term placentas from 88 malaria-infected and -noninfected Cameroon women. Interleukin (IL)-2 and-4 were consistently low ; IL-1Beta, IL-6, granulocyte-macrophage colony-stimulating factor, and transforming growth factor (TGF)-Beta2 were highest in PBC cultures. Malaria placental infection increased Th1-type cytokines, whereas Th-type cytokines and TGF-Beta2 were unchanged. Addition of lipopolysaccharide or infected erythrocytes to cultures increased TNF-alpha, IL-1Beta, IL-6,and IL-10 secretions but not those of IFN-gamma and IL-4. Overall, #Plasmodium falciparum$ induced a placental immune response involving both Th1- and Th2-type cell activation. Although the Th1 pathway was favored, IL-10 secretion was also increased, and this increase should be effective in protecting the placenta by controlling the negative effects of Th1 cytokines on pregnancy. (Résumé d'auteur)</abstract>
      <custom6>052ANOPAL03</custom6>
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