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      <src>https://www.socictopen.socict.org/files/original/4d0d543490f325763eedbc576dbe8fd0.pdf</src>
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          <element elementId="50">
            <name>Title</name>
            <description>A name given to the resource</description>
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                <text>Coronavirus</text>
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            <name>Description</name>
            <description>An account of the resource</description>
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                <text>Dominio científico: Coronavirus</text>
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            </elementTextContainer>
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    <name>Text</name>
    <description>A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.</description>
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      <name>Dublin Core</name>
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        <element elementId="50">
          <name>Title</name>
          <description>A name given to the resource</description>
          <elementTextContainer>
            <elementText elementTextId="21367">
              <text>Toll-like receptors, chemokine receptors and death receptor ligands responses in SARS coronavirus infected human monocyte derived dendritic cells</text>
            </elementText>
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        </element>
        <element elementId="39">
          <name>Creator</name>
          <description>An entity primarily responsible for making the resource</description>
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            <elementText elementTextId="21368">
              <text>Law Helen KW, Cheung Chung, Sia Sin, Chan Yuk, Peiris JS Malik, Lau Yu</text>
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        <element elementId="41">
          <name>Description</name>
          <description>An account of the resource</description>
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              <text>Abstract Background The SARS outbreak in 2003 provides a unique opportunity for the study of human responses to a novel virus. We have previously reported that dendritic cells (DCs) might be involved in the immune escape mechanisms for SARS-CoV. In this study, we focussed on the gene expression of toll-like receptors (TLRs), chemokine receptors (CCRs) and death receptor ligands in SARS-CoV infected DCs. We also compared adult and cord blood (CB) DCs to find a possible explanation for the age-dependent severity of SARS. Results Our results demonstrates that SARS-CoV did not modulate TLR-1 to TLR-10 gene expression but significantly induced the expression of CCR-1, CCR-3, and CCR-5. There was also strong induction of TNF-related apoptosis-inducing ligand (TRAIL), but not Fas ligand gene expression in SARS-CoV infected DCs. Interestingly, the expressions of most genes studied were higher in CB DCs than adult DCs. Conclusion The upregulation of chemokines and CCRs may facilitate DC migration from the infection site to the lymph nodes, whereas the increase of TRAIL may induce lymphocyte apoptosis. These findings may explain the increased lung infiltrations and lymphoid depletion in SARS patients. Further explorations of the biological significance of these findings are warranted.</text>
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          <name>Date</name>
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              <text>2009</text>
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          <name>Identifier</name>
          <description>An unambiguous reference to the resource within a given context</description>
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              <text>DOI: 10.1186/1471-2172-10-35</text>
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          <name>Source</name>
          <description>A related resource from which the described resource is derived</description>
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            <elementText elementTextId="21372">
              <text>BMC Immunology</text>
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          <name>Publisher</name>
          <description>An entity responsible for making the resource available</description>
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            <elementText elementTextId="21373">
              <text>BMC</text>
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          </elementTextContainer>
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          <name>Coverage</name>
          <description>The spatial or temporal topic of the resource, the spatial applicability of the resource, or the jurisdiction under which the resource is relevant</description>
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            <elementText elementTextId="21374">
              <text>Immunologic diseases. Allergy</text>
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          </elementTextContainer>
        </element>
        <element elementId="44">
          <name>Language</name>
          <description>A language of the resource</description>
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            <elementText elementTextId="21375">
              <text>EN</text>
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