American Journal of Tropical Medicine and Hygiene · 1998 · 33 citations · 13 references
Veterinary MedicineImmunologyInfectious DiseasesHost-pathogen InteractionsImmunology Of Infectious DiseasesImmunopathologyChagas DiseaseHost-parasite Immune InteractionsParasitic Disease PathogenesisProtozoal InfectionsProtozoan Host-parasite InteractionsT-cell Responses To ParasitesAcute Chagas DiseaseChagas CardiomyopathyChronic Chagas DiseaseImmunopathology Of TrypanosomiasisT Helper Cell CytokinesTrypanosoma Cruzi InfectionTrypanosomatid-host InteractionsTrypanosome Infections
Both parasite and host immune factors may contribute to the development and progression of chronic chagasic cardiomyopathy during Trypanosoma cruzi infections. The present study targeted infected children (5-14 years of age) from an endemic area of Paraguay in an analysis of T. cruzi-specific cytokine profiles. This age group is characteristically the most affected by the early phases of infection. Trypanosoma cruzi-induced cytokine gene expression (interleukin-2 [IL-2], and interferon-gamma [IFN-gamma], IL-4, and IL-10) was studied in 25 seropositive children categorized as being either acute, symptomatic, with Romana's sign (n = 2), or early, indeterminate (postacute, n = 23). Acutely infected children showed a distinct T helper cell-1 (Th1)-type (IFN-gamma) cytokine response to infection. The cytokine pattern that was observed in the seropositive, asymptomatic (early, indeterminate) group was of the Th0 type (expression of both IFN-gamma and IL-4). We hypothesize that selective induction of a Th0-type cytokine pattern is important for development of cell-mediated and humoral immune responses that suppress parasite burden, thereby prolonging the onset or limiting the severity of chronic Chagas' disease later in life.
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Ricardo T. Gazzinelli, Maria Wysocka, Sara Hieny et al. · The Journal of Immunology · 1996 · 929 citations · Full text
João S. Silva, G N R Vespa, Júlio Aliberti et al. · Infection and Immunity · 1995 · 320 citations · Full text