IL-10 limits parasite burden and protects against fatal myocarditis in a mouse model of Trypanosoma cruzi infection

dc.creatorRoffê, Ester
dc.creatorRothfuchs, Antonio Gigliotti
dc.creatorSantiago, Helton da Costa
dc.creatorMarino, Ana Paula Maia Peixoto
dc.creatorGomes, Flavia Lima Ribeiro
dc.creatorEckhaus, Michael
dc.creatorAntonelli, Lis Ribeiro do Valle
dc.creatorMurphy, Philip M.
dc.date2014-06-27T14:20:48Z
dc.date2014-06-27T14:20:48Z
dc.date2012
dc.date.accessioned2023-09-26T22:22:28Z
dc.date.available2023-09-26T22:22:28Z
dc.identifierROFFE, Ester et al. IL-10 limits parasite burden and protects against fatal myocarditis in a mouse model of Trypanosoma cruzi infection. The Journal of Immunology. 2012, vol.188, pp. 649-660
dc.identifier0022-1767
dc.identifierhttps://www.arca.fiocruz.br/handle/icict/7844
dc.identifier.urihttps://repositorioslatinoamericanos.uchile.cl/handle/2250/8878438
dc.descriptionChagas' disease is a zoonosis prevalent in Latin America that is caused by the protozoan Trypanosoma cruzi. The immunopathogenesis of cardiomyopathy, the main clinical problem in Chagas' disease, has been extensively studied but is still poorly understood. In this study, we systematically compared clinical, microbiologic, pathologic, immunologic, and molecular parameters in two mouse models with opposite susceptibility to acute myocarditis caused by the myotropic Colombiana strain of T. cruzi: C3H/HeSnJ (100% mortality, uncontrolled parasitism) and C57BL/6J (<10% mortality, controlled parasitism). T. cruzi induced differential polarization of immunoregulatory cytokine mRNA expression in the hearts of C57BL/6J versus C3H/HeSnJ mice; however, most differences were small. The difference in IL-10 expression was exceptional (C57BL/6J 8.7-fold greater than C3H/HeSnJ). Consistent with this, hearts from infected C57BL/6J mice, but not C3H/HeSnJ mice, had a high frequency of total IL-10-producing CD8(+) T cells and both CD4(+) and CD8(+) subsets of IFN-γ(+)IL-10(+) double-producing T cells. Furthermore, T. cruzi infection of IL-10(-/-) C57BL/6J mice phenocopied fatal infection in wild-type C3H/HeSnJ mice with complete loss of parasite control. Adoptive transfer experiments indicated that T cells were a source of protective IL-10. Thus, in this system, IL-10 production by T cells promotes T. cruzi control and protection from fatal acute myocarditis.
dc.formatapplication/pdf
dc.languageeng
dc.publisherThe American Association of Immunologists
dc.rightsopen access
dc.subjectChagas Disease/mortality
dc.subjectInterleukin-10/deficiency
dc.subjectInterleukin-10/physiology
dc.subjectMice, Inbred C3H
dc.subjectMyocarditis/parasitology
dc.subjectMyocarditis/prevention & control
dc.titleIL-10 limits parasite burden and protects against fatal myocarditis in a mouse model of Trypanosoma cruzi infection
dc.typeArticle


Este ítem pertenece a la siguiente institución