Article
Complement C2 receptor inhibitor trispanning confers an increased ability to resist complement-mediated lysis in Trypanosoma cruzi
Registro en:
CESTARI, Igor dos S. et al. Complement C2 Receptor Inhibitor Trispanning Confers an Increased Ability to Resist Complement- Mediated Lysis in Trypanosoma cruzi. The Journal of Infectious Diseases, v. 198, p.1276–1283, 2008.
0022-1899
10.1086/592167
1537-6613
Autor
Cestari, Igor dos S.
Evans-Osses, Ingrid
Freitas, Juliana C.
Inal, Jameel M.
Ramirez, Marcel I.
Resumen
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. 2022-01-01
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