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dc.contributor.authorCestari, Igor Dos S
dc.contributor.authorEvans-Osses, Ingrid
dc.contributor.authorFreitas, Juliana C
dc.contributor.authorInal, Jameel M
dc.contributor.authorRamirez, Marcel I
dc.identifier.citationCestari , I D S , Evans-Osses , I , Freitas , J C , Inal , J M & Ramirez , M I 2008 , ' Complement C2 receptor inhibitor trispanning confers an increased ability to resist complement-mediated lysis in Trypanosoma cruzi ' , Journal of Infectious Diseases , vol. 198 , no. 9 , pp. 1276-83 .
dc.identifier.otherPURE: 13069589
dc.identifier.otherPURE UUID: 7b5b0897-4b37-488c-b91c-5e4e96c2bd60
dc.identifier.otherPubMed: 18781865
dc.identifier.otherScopus: 54249162286
dc.description.abstractThe ability to resist complement differs between the Y and Colombiana Trypanosoma cruzi strains. We found that the Y strain of T. cruzi was more able to resist the classical and lectin pathways of complement activation than the Colombiana strain. The complement C2 receptor inhibitor trispanning gene (CRIT) is highly conserved in both strains. At the protein level, CRIT is expressed only in stationary-phase epimastigotes of the Y but not the Colombiana strain and is expressed in infectious metacyclic trypomastigotes of both strains. Y strain epimastigotes with an overexpressed CRIT gene (pTEX-CRIT) had higher survival in normal human serum (NHS). Overexpression of the Y strain CRIT gene in Colombiana epimastigote forms increased the parasite's resistance to lysis mediated by the classical and lectin pathways but not to lysis mediated by alternative pathways. CRIT involvement on the parasite surface was confirmed by showing that the lytic activity of NHS against epimastigotes could be restored by adding excess C2.en
dc.relation.ispartofJournal of Infectious Diseases
dc.subjectAmino Acid Sequence
dc.subjectCloning, Molecular
dc.subjectComplement System Proteins
dc.subjectGene Expression Regulation
dc.subjectMolecular Biology
dc.subjectMolecular Sequence Data
dc.subjectOrganisms, Genetically Modified
dc.subjectProtozoan Proteins
dc.subjectReceptors, Cell Surface
dc.subjectTrypanosoma cruzi
dc.subjectJournal Article
dc.subjectResearch Support, Non-U.S. Gov't
dc.titleComplement C2 receptor inhibitor trispanning confers an increased ability to resist complement-mediated lysis in Trypanosoma cruzien
dc.contributor.institutionSchool of Life and Medical Sciences
dc.description.statusPeer reviewed
rioxxterms.typeJournal Article/Review

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