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    <titleInfo>
      <title>#Plasmodium falciparum$ induces a Th1/Th2 disequilibrium, favoring the Th1-type pathway, in the human placenta</title>
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      <namePart type="family">Fievet</namePart>
      <namePart type="given">Nadine</namePart>
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      <namePart type="family">Tami</namePart>
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    <name type="personnal">
      <namePart type="family">Maubert</namePart>
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        <roleTerm type="text">auteur</roleTerm>
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      <namePart type="family">Cot</namePart>
      <namePart type="given">Michel</namePart>
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    <name type="personnal">
      <namePart type="family">Deloron</namePart>
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    <name type="personnal">
      <namePart type="family">Chaouat</namePart>
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    <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>
    <targetAudience authority="marctarget">specialized</targetAudience>
    <subject authority="local">
      <topic>PALUDISME</topic>
      <topic>AGENT PATHOGENE</topic>
      <topic>FEMME</topic>
      <topic>GROSSESSE</topic>
      <topic>IMMUNITE</topic>
      <topic>IMMUNOLOGIE</topic>
      <topic>CELLULE</topic>
      <topic>CULTURE IN VITRO</topic>
      <topic>ETUDE EXPERIMENTALE</topic>
    </subject>
    <subject>
      <topic>TRANSMISSION PLACENTAIRE</topic>
      <topic>TH1 CYTOKINE</topic>
      <topic>TH2 CYTOKINE</topic>
    </subject>
    <subject authority="local">
      <geographic>CAMEROUN</geographic>
      <geographic>YAOUNDE</geographic>
    </subject>
    <classification authority="local">052ANOPAL03</classification>
    <relatedItem type="host">
      <titleInfo>
        <title>Journal of Infectious Diseases</title>
      </titleInfo>
      <part>
        <detail type="volume">
          <number>183</number>
        </detail>
        <detail type="volume">
          <number>10</number>
        </detail>
        <extent unit="pages">
          <list> 1530-1534</list>
        </extent>
      </part>
      <originInfo>
        <dateIssued>2001</dateIssued>
      </originInfo>
      <identifier type="issn">0002-1899</identifier>
    </relatedItem>
    <identifier type="uri">https://www.documentation.ird.fr/hor/fdi:010025993</identifier>
    <identifier type="doi">10.1086/320201</identifier>
    <identifier type="issn">0002-1899</identifier>
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      <url usage="primary display" access="object in context">https://www.documentation.ird.fr/hor/fdi:010025993</url>
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      <recordCreationDate encoding="w3cdtf">2001-08-21</recordCreationDate>
      <recordChangeDate encoding="w3cdtf">2018-08-17</recordChangeDate>
      <recordIdentifier>fdi:010025993</recordIdentifier>
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        <languageTerm authority="iso639-2b">fre</languageTerm>
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