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      <ref-type name="Journal Article">17</ref-type>
      <work-type>ACL : Articles dans des revues avec comité de lecture répertoriées par l'AERES</work-type>
      <contributors>
        <authors>
          <author>
            <style face="normal" font="default" size="100%">Turner, J. D.</style>
          </author>
          <author>
            <style face="normal" font="default" size="100%">Faulkner, H.</style>
          </author>
          <author>
            <style face="bold" font="default" size="100%">Kamgno, J.</style>
          </author>
          <author>
            <style face="normal" font="default" size="100%">Kennedy, M. W.</style>
          </author>
          <author>
            <style face="normal" font="default" size="100%">Behnke, J.</style>
          </author>
          <author>
            <style face="bold" font="default" size="100%">Boussinesq, M.</style>
          </author>
          <author>
            <style face="normal" font="default" size="100%">Bradley, J. E.</style>
          </author>
        </authors>
      </contributors>
      <titles>
        <title>Allergen-specific IgE and IgG4 are markers of resistance and susceptibility in a human intestinal nematode infection</title>
        <secondary-title>Microbes and Infection</secondary-title>
      </titles>
      <pages>990-996</pages>
      <keywords>
        <keyword>IgE</keyword>
        <keyword>IgG4</keyword>
        <keyword>allergen</keyword>
        <keyword>helminth</keyword>
        <keyword>immunity</keyword>
        <keyword>Th2</keyword>
      </keywords>
      <dates>
        <year>2005</year>
      </dates>
      <call-num>PAR00000409</call-num>
      <language>ENG</language>
      <periodical>
        <full-title>Microbes and Infection</full-title>
      </periodical>
      <isbn>1286-4579</isbn>
      <accession-num>CC:0002309792-0004</accession-num>
      <number>7-8</number>
      <electronic-resource-num>10.1016/j.micinf.2005.03.036</electronic-resource-num>
      <urls>
        <related-urls>
          <url>https://www.documentation.ird.fr/hor/PAR00000409</url>
        </related-urls>
      </urls>
      <volume>7</volume>
      <remote-database-provider>Horizon (IRD)</remote-database-provider>
      <abstract>IgG4 has been proposed to act as a 'blocking antibody' due to its ability to compete for the same epitopes as IgE thus preventing IgE-dependent allergic responses. IgG4 and IgE are both elevated in helminth infections and strong anti-parasite IgE responses are associated with resistance to infection. We wished to determine the relationship between anti-parasite IgG4 and IgE and Ascaris lumbricoides infection status. We examined anti-parasite responses, including antibody levels to recombinant Ascaris allergen-1A (rABA-1A), a target of serum IgE in endemic populations. Worm burden was indirectly estimated by measuring parasite egg output in a cross-sectional human population (N = 105). Levels of anti-parasite IgG4 and IgE in patients' plasma were quantified by immunoassay. Global anti-parasite antibody responses did not bear any significant relationships with intensity of Ascaris infection. Individuals who had detectable levels of IgE but not IgG4 to rABA-1A (11%) had lower average levels of infection compared with individuals who produced anti-rABA-1A IgG4 (40%) and sero-negative individuals (49%) (P = 0.008). The ratio of IgG4/IgE in rABA-1A responders positively correlated with intensity of infection (P &lt; 0.025). IgG4 levels positively correlated with infection level in younger children (age 4-11) where average levels of infection were increasing (P = 0.038), whereas allergen specific IgE emerged as a correlate of immunity in older children and adults (age 12-36) where infection levels were decreasing (P = 0.048). Therefore, in a gastrointestinal helminth infection, differential regulation of anti-allergen antibody isotypes relate to infection level. Our results are consistent with the concept that IgG4 antibody can block IgE-mediated immunity and therefore allergic processes in humans. (c) 2005 Elsevier SAS. All rights reserved.</abstract>
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