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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%">Sabbagh, A.</style>
          </author>
          <author>
            <style face="normal" font="default" size="100%">Sonon, P.</style>
          </author>
          <author>
            <style face="normal" font="default" size="100%">Sadissou, I.</style>
          </author>
          <author>
            <style face="normal" font="default" size="100%">Mendes, C. T.</style>
          </author>
          <author>
            <style face="bold" font="default" size="100%">Garcia, André</style>
          </author>
          <author>
            <style face="normal" font="default" size="100%">Donadi, E. A.</style>
          </author>
          <author>
            <style face="bold" font="default" size="100%">Courtin, David</style>
          </author>
        </authors>
      </contributors>
      <titles>
        <title>The role of HLA-G in parasitic diseases</title>
        <secondary-title>HLA</secondary-title>
      </titles>
      <pages>255-270</pages>
      <keywords>
        <keyword>echinococcosis</keyword>
        <keyword>genetics</keyword>
        <keyword>HLA-G</keyword>
        <keyword>immune system</keyword>
        <keyword>leishmaniosis</keyword>
        <keyword>malaria</keyword>
        <keyword>parasite</keyword>
        <keyword>toxoplasmosis</keyword>
        <keyword>trypanosomiasis</keyword>
        <keyword>AFRIQUE SUBSAHARIENNE</keyword>
        <keyword>AMERIQUE LATINE</keyword>
      </keywords>
      <dates>
        <year>2018</year>
      </dates>
      <call-num>fdi:010072479</call-num>
      <language>ENG</language>
      <periodical>
        <full-title>HLA</full-title>
      </periodical>
      <isbn>2059-2302</isbn>
      <accession-num>ISI:000427474300001</accession-num>
      <number>4</number>
      <electronic-resource-num>10.1111/tan.13196</electronic-resource-num>
      <urls>
        <related-urls>
          <url>https://www.documentation.ird.fr/hor/fdi:010072479</url>
        </related-urls>
        <pdf-urls>
          <url>https://www.documentation.ird.fr/intranet/publi/2018/04/010072479.pdf</url>
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      </urls>
      <volume>91</volume>
      <remote-database-provider>Horizon (IRD)</remote-database-provider>
      <abstract>Little attention has been devoted to the role of HLA-G gene and molecule on parasitic disorders, and the available studies have focused on malaria, African and American trypanosomiasis, leishmaniosis, toxoplasmosis and echinococcosis. After reporting a brief description regarding the role of the cells of innate and adaptive immune system against parasites, we reviewed the major features of the HLA-G gene and molecule and the role of HLA-G on the major cells of immune system. Increased levels of soluble HLA-G (sHLA-G) have been observed in patients presenting toxoplasmosis and in the active phase of echinococcosis. In addition, increased sHLA-G has also been associated with increased susceptibility to malaria and increased susceptibility to develop human African trypanosomiasis (HAT). In contrast, decreased membrane-bound HLA-G has been reported in placenta of patients infected with Plasmodium falciparum and in heart and colon of patients presenting Chagas disease. The 30 untranslated region of the HLA-G gene has been the main focus of studies on malaria, HAT and Chagas disease, exhibiting distinct patterns of associations. Considering that HLA-G is an immune checkpoint molecule, inhibiting the activity of several cells of the immune system, the excessive neoexpression and the increased sHLA-G levels together with the decreased constitutive tissue expression of membrane-bound HLA-G may be detrimental to the host infected with parasite agents.</abstract>
      <custom6>052 ; 050</custom6>
      <custom1>UR216</custom1>
      <custom7>Bénin / Brésil</custom7>
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