Garzon Edwin auteur aut IRD Genna F. auteur aut IRD Bosseno Marie-France auteur aut IRD Simony La Fontaine J. auteur aut IRD Radal M. auteur aut IRD Séréno Denis auteur aut IRD Mathieu Daudé Françoise auteur aut IRD Ouaissi Ali auteur aut IRD Brenière Simone Frédérique auteur aut IRD text journalArticle eng Immunopathology of Chagas' disease in Balb/c mice infected with 2 Trypanosoma cruzi clones, belonging to the T. cruzi I lineage and presenting different in vitro virulence (P/209 ell > SO34 c14) was compared. In the acute phase, evading mechanisms such as parasite-induced lymphocyte polyclonal activation and T cell immunosuppression were higher in mice infected with the clone giving a higher parasitaemia (P/209 c11). A similar increase of non-specific isotypes was observed in both infections with IgG2a prevalence. Interestingly, CD8+ cell hypercellularity and lymphocyte immunosuppression were observed during the chronic phase (245 days post-infection) in mice infected by the most virulent clone. In the same way, the parasite-specific antibody response was more intense in P/209 c11-infected mice over the acute phase. During the chronic phase this response remarkably dropped down in SO34 c14-infected mice exclusively. Finally, P/209 ell-infected mice presented a more severe inflammation and tissue damage in heart and quadriceps than SO34 c14-infected mice. This comparative study showed differences between the two clones: a higher virulence in vivo being clearly associated with a greater ability to induce evasion mechanisms and severe tissue damage. specialized Trypanosoma cruzi genotype immunopathology virulence mouse 052 131 Part 1 109-119 2005 0031-1820 https://www.documentation.ird.fr/hor/fdi:010041532 10.1017/S003118200400722X 0031-1820 [F B010041532] https://www.documentation.ird.fr/hor/fdi:010041532 IRD - Base Horizon / Pleins textes 2006-03-29 2017-08-23 fdi:010041532 fre