Complement C2 receptor inhibitor trispanning confers an increased ability to resist complement-mediated lysis in Trypanosoma cruzi.
The 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.
Cestari
Igor Dos S
Idos S
Departamento de Bioquímica e Biologia Molecular, Instituto Oswaldo Cruz (Fiocruz), Rio de Janeiro, Brazil.
Evans-Osses
Ingrid
I
Freitas
Juliana C
JC
Inal
Jameel M
JM
Ramirez
Marcel I
MI
D000595:Amino Acid Sequence; D000818:Animals; D003001:Cloning, Molecular; D003165:Complement System Proteins / Q000494:pharmacology*; D005786:Gene Expression Regulation / Q000502:physiology; D008967:Molecular Biology; D008969:Molecular Sequence Data; D030781:Organisms, Genetically Modified; D015800:Protozoan Proteins / Q000378:metabolism*; D011956:Receptors, Cell Surface; D014349:Trypanosoma cruzi / Q000145:classification / Q000187:drug effects* / Q000235:genetics / Q000378:metabolism*
D015800:Protozoan Proteins; D011956:Receptors, Cell Surface; D003165:Complement System Proteins