Journal of Biomedicine and Biotechnology · 2010 · 55 citations · 41 references
Veterinary MedicineImmunologyInfectious DiseasesHost-pathogen InteractionsImmunology Of Infectious DiseasesParasite ImmunologyCell-mediated ImmunityCellular Immune ResponsesCellular Immunity In InfectionHost-parasite Immune InteractionsHumoral Immune ResponsesT-cell Responses To ParasitesCellular Inflammatory ResponsesImmunoglobulin ResponsesImmunopathology Of TrypanosomiasisLymphocytic InfiltratesParasite-immune InteractionsTh1 Immune ResponseTrypanosoma Cruzi InfectionTrypanosomatid-host Interactions
It is has been shown that the majority of T. cruzi strains isolated from Mexico belong to the T. cruzi I (TCI). The immune response produced in response to Mexican T. cruzi I strains has not been well characterized. In this study, two Mexican T. cruzi I strains were used to infect Balb/c mice. The Queretaro (TBAR/MX/0000/Queretaro)(Qro) strain resulted in 100% mortality. In contrast, no mortality was observed in mice infected with the Ninoa (MHOM/MX/1994/Ninoa) strain. Both strains produced extended lymphocyte infiltrates in cardiac tissue. Ninoa infection induced a diverse humoral response with a higher variety of immunoglobulin isotypes than were found in Qro-infected mice. Also, a stronger inflammatory TH1 response, represented by IL-12p40, IFNgamma, RANTES, MIG, MIP-1beta, and MCP-1 production was observed in Qro-infected mice when compared with Ninoa-infected mice. We propose that an exacerbated TH1 immune response is a likely cause of pathological damage observed in cardiac tissue and the primary cause of death in Qro-infected mice.
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Matthew Yeo, Nidia Acosta, Martin Llewellyn et al. · International Journal for Parasitology · 2004 · 304 citations
Júlio Aliberti, Gislâine A. Martins, Ricardo T. Gazzinelli et al. · Infection and Immunity · 1996 · 287 citations · Full text