<rdf:RDF xmlns:rdf="http://www.w3.org/1999/02/22-rdf-syntax-ns#" xmlns:dcterms="http://purl.org/dc/terms/">
<rdf:Description rdf:about="https://riquim.fq.edu.uy/items/show/5650">
    <dcterms:title><![CDATA[<strong>Antigen B from Echinococcus granulosus is a novel ligand for C-reactive protein</strong>]]></dcterms:title>
    <dcterms:subject><![CDATA[PROTEINAS]]></dcterms:subject>
    <dcterms:subject><![CDATA[PROTEINA C REACTIVA]]></dcterms:subject>
    <dcterms:subject><![CDATA[ECHINOCOCCUS GRANULOSUS]]></dcterms:subject>
    <dcterms:subject><![CDATA[MACROFAGOS]]></dcterms:subject>
    <dcterms:subject><![CDATA[BIBLIOGRAFIA NACIONAL QUIMICA]]></dcterms:subject>
    <dcterms:subject><![CDATA[2018]]></dcterms:subject>
    <dcterms:abstract><![CDATA[Antigen B (EgAgB) is a phosphatidylcholine (PC)-rich lipoprotein of Echinococcus granulosus s.l. larva, potentially capable of modulating the activation of various myeloid cells, including macrophages. As C-reactive protein (CRP) can act as an innate receptor with ability to bind the phosphocholine moiety of PC in lipoproteins, we investigated whether EgAgB and CRP could interact during cystic echinococcosis infection (CE), and how CRP binding could affect the modulation activities exerted by EgAgB on macrophages. To that end, we firstly investigated the occurrence of CRP induction during human CE. We found that 61% of CE patients, but none of healthy donors, exhibited serum CRP levels higher than 10 mg/mL, suggesting that CRP can be induced during the chronic phase of CE. Furthermore, human CRP was capable of binding specifically to EgAgB with high affinity (0.6 &plusmn; 0.1 nM); this binding was Ca2+ -dependent and involved the phosphocholine moiety of PC, but not EgAgB8/1, EgAgB8/2 or EgAgB8/3 apolipoproteins. Finally, CRP presence altered the modulation exerted by EgAgB on the cytokine response of LPS-activated macrophages. Overall, our results suggest that CRP presence during CE may contribute to a complex scenario of interactions between EgAgB and myeloid cells, influencing the cytokine response induced during macrophage activation.]]></dcterms:abstract>
    <dcterms:creator><![CDATA[<strong>Silva-Alvarez, Valeria</strong>]]></dcterms:creator>
    <dcterms:creator><![CDATA[<strong>Ramos, Anal&iacute;a</strong>]]></dcterms:creator>
    <dcterms:creator><![CDATA[<strong>Folle, Ana Maite</strong>]]></dcterms:creator>
    <dcterms:creator><![CDATA[<strong>Lagos, Sof&iacute;a.</strong>]]></dcterms:creator>
    <dcterms:creator><![CDATA[<strong>Dee, Valerie M.</strong>]]></dcterms:creator>
    <dcterms:creator><![CDATA[<strong>Ferreira, Ana M.</strong>]]></dcterms:creator>
    <dcterms:source><![CDATA[Parasite Immunology&nbsp; v. 40, no. 9, 2018. -- 6p.--e12575]]></dcterms:source>
    <dcterms:publisher><![CDATA[Wiley]]></dcterms:publisher>
    <dcterms:date><![CDATA[2018]]></dcterms:date>
    <dcterms:rights><![CDATA[<p><strong>Informaci&oacute;n sobre Derechos de Autor</strong></p>
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<p><strong>ADVERTENCIA -</strong> La consulta de este documento queda condicionada a la aceptaci&oacute;n de las siguientes condiciones de uso: Este documento es &uacute;nicamente para usos privados enmarcados en actividades de investigaci&oacute;n y docencia. No se autoriza su reproducci&oacute;n con fines de lucro. Esta reserva de derechos afecta tanto los datos del documento como a sus contenidos. En la utilizaci&oacute;n o cita de partes debe indicarse el nombre de la persona autora.</p>]]></dcterms:rights>
    <dcterms:format><![CDATA[PDF]]></dcterms:format>
    <dcterms:language><![CDATA[Ingl&eacute;s]]></dcterms:language>
    <dcterms:type><![CDATA[Art&iacute;culo]]></dcterms:type>
    <dcterms:identifier><![CDATA[DOI:10.1111/pim.12575]]></dcterms:identifier>
</rdf:Description></rdf:RDF>
