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    <!-- http://purl.obolibrary.org/obo/EUPATH_0000737 -->

    <Class rdf:about="http://purl.obolibrary.org/obo/EUPATH_0000737">
        <rdfs:label xml:lang="en">cluster of differentiation 36 genotype</rdfs:label>
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        <ns2:EUPATH_0000052>CD36 genotype</ns2:EUPATH_0000052>
        <ns2:IAO_0000115 xml:lang="en">A genotype information which is about  cluster of differentiation 36 (CD36) gene, which encodes an integral membrane protein in many cell types and a member of the scavenger receptor family that imports fatty acids into cells (Canton et al., 2013). CD36 is also an endothelial receptor for binding of erythrocytes infected with P. falciparum.</ns2:IAO_0000115>
        <ns2:IAO_0000116>Grant Dorsey: The human CD36 antigen is an integral membrane protein in many cell types and a member of the scavenger receptor family that imports fatty acids into cells (Canton et al., 2013). CD36 is also an endothelial receptor for binding of erythrocytes infected with P. falciparum; this cytoadhesion is believed to be an important feature of the virulence of falciparum malaria, due both to its prevention of clearance of infected erythrocytes by the spleen and to local effects of cytoadhering parasites (Newbold et al., 1999). Importantly, expression of CD36 is low in the brain, even in the setting of cerebral malaria (Silamut et al., 1999), suggesting that binding to CD36 is most relevant in non-cerebral forms of severe malaria. CD36 is also believed to be an important macrophage pattern recognition receptor that mediates innate recognition and clearance of infected erythrocytes (Cabrera et al., 2014). Considering our current understanding, CD36 expression might be seen to contribute to malaria severity, by mediating cytoadherence, or to help control malaria, via immune effects. Results with murine malaria models have been complex; mice with decreased CD36-mediated cytoadherence had decreased growth of P. berghei (Fonager et al., 2012), but CD36-deficient mice had increased risk of fatal P. chabaudi malaria (Patel et al., 2007). Considering human populations, many CD36 polymorphisms, including nonsense mutations that prevent production of the molecule, are common, particularly in African populations (Aitman et al., 2000). However, attempts to identify associations between common polymorphisms and malaria risk have led to inconsistent results, with evidence for enhancement of(Aitman et al., 2000; Omi et al., 2002), no effect (Fry et al., 2009), or protection from (Das et al., 2009; Omi et al., 2003; Pain et al., 2001; Sinha et al., 2008) severe malaria with different polymorphisms.
CD3T188G is a polymophism on the human CD36 gene.</ns2:IAO_0000116>
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