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Complement C2 receptor inhibitor trispanning confers an increased ability to resist complement-mediated lysis in Trypanosoma cruzi

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contributor authorCestari, Igor Dos S
contributor authorEvans-Osses, Ingrid
contributor authorFreitas, Juliana C
contributor authorInal, Jameel M
contributor authorRamirez, Marcel I
date accessioned2018-07-31T14:30:35Z
date available2018-07-31T14:30:35Z
date issued2008-11-01
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 . DOI: 10.1086/592167en
identifier issn0022-1899
identifier otherPURE: 13069589
identifier otherPURE UUID: 7b5b0897-4b37-488c-b91c-5e4e96c2bd60
identifier otherPubMed: 18781865
identifier otherScopus: 54249162286
identifier urihttp://hdl.handle.net/2299/20316
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
format extent8en
language isoeng
relation ispartofJournal of Infectious Diseasesen
rightsen
subjectAmino Acid Sequenceen
subjectAnimalsen
subjectCloning, Molecularen
subjectComplement System Proteinsen
subjectGene Expression Regulationen
subjectMolecular Biologyen
subjectMolecular Sequence Dataen
subjectOrganisms, Genetically Modifieden
subjectProtozoan Proteinsen
subjectReceptors, Cell Surfaceen
subjectTrypanosoma cruzien
subjectJournal Articleen
subjectResearch Support, Non-U.S. Gov'ten
titleComplement C2 receptor inhibitor trispanning confers an increased ability to resist complement-mediated lysis in Trypanosoma cruzien
typeArticleen
contributor institutionSchool of Life and Medical Sciencesen
identifier doihttps://doi.org/10.1086/592167
description statusPeer revieweden


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