Please use this identifier to cite or link to this item: https://www.arca.fiocruz.br/handle/icict/19737
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dc.contributor.authorCardillo, Fabíola
dc.contributor.authorCunha, Fernando de Queiroz
dc.contributor.authorTamashiro, Wirla Maria da Silva Cunha
dc.contributor.authorRusso, Momtchilo
dc.contributor.authorGarcia, S. B
dc.contributor.authorMengele Junior, José Orivaldo
dc.date.accessioned2017-07-06T12:30:15Z
dc.date.available2017-07-06T12:30:15Z
dc.date.issued2002
dc.identifier.citationCARDILLO, F. et al. NK1.1+ cells and T-cell activation in euthymic and thymectomized C57BL/6 mice during acute Trypanosoma cruzi infection. Scandinavian Journal of Infection, v. 55, n. 1, p. 96-104, 2002.
dc.identifier.issn0300-9475
dc.identifier.urihttps://www.arca.fiocruz.br/handle/icict/19737
dc.descriptionCardillo, Fabíola; Mengel Junior, Jose Orivaldo “Documento produzido em parceria ou por autor vinculado à Fiocruz, mas não consta à informação no documento”.
dc.description.sponsorshipFAPESP, CNPq
dc.language.isoeng
dc.publisherWiley
dc.rightsopen access
dc.subject.otherTrypanosoma cruzi
dc.subject.otherInfecção
dc.subject.otherCélulas NK
dc.subject.otherAnimais
dc.subject.otherCamundongos
dc.titleNK1.1+ cells and T-cell activation in euthymic and thymectomized C57BL/6 mice during acute Trypanosoma cruzi infection
dc.typeArticle
dc.description.abstractenNatural killer (NK) cells may provide the basis for resistance to Trypanosoma cruzi infection, because the depletion of NK1.1 cessla causes high levels of parasitemia in Young C57B1/6 mice infected with T. cruzi. Indeed, NK1.1 cells have been implicated in the early production of large amounts of interferon (IFN)-y, na importante cytokine in host resistance. The NK.1 marker is also expressed on special subpopulations of T cells. Most NK1.1+ T cells are of thymic origin, and their constant generation may be prevented by thymectomy. This procedure, by itself, decreased parasitemia and increased resistance in young mice. However, the depletion of NK1.1+ cells by the chronic administration of a monoclonal antibody (MoAb) (PK-136) did not increase the parasitemia or mortality in thymectomized C57B1/6 mice infected with T. cruzi (Tulahuen strain). To study the cross-talk between NK1.1+ cells and conventional T cells in this model, we examined the expression. of activation/memory markers (CD45RB) on splenic CD4+ and CD8+ T cells from Young euthymic or thymectomized mice with or without depletion of NK1.1+ cells and also in aged mice during acute infection. Resistance to infection correlated with the amount of CD4+ T cells that are already acitivated at the moment of infection, as judged by the number of splenic CD4+ T cells expressing CD45RB-. In addition, the specific antibody response to T cruzi antigens was precocious and na accumulation of immunoglobulin (Ig)M with little isotype switch occurred in euthymic mice depleted of NK1.1+ cells. The data presented here suggest that NK1.1+ cells have importante regulatory functions in euthymic, but not in thymectomized mice infected with T. cruzi. These regulatory functions include a helper activity in the generation of effector or activated/mewmory T cells.
dc.creator.affilliationUniversity of São Paulo. Institute of Biomedical Sciences-IV. Department of Immunology. São Paulo, SP, Brazil
dc.creator.affilliationUniversity of Sao Paulo. Faculty of Ribeirão Preto. Department of Pharmacology. Ribeirão Preto, SP, Brazil
dc.creator.affilliationUniversity of Campinas. Institute for Biology. Department of Microbiology and Immunology. Campinas, SP, Brazil
dc.creator.affilliationUniversity of São Paulo. Institute of Biomedical Sciences-IV. Department of Immunology. São Paulo, SP, Brazil
dc.creator.affilliationUniversity of São Paulo. Faculty of Medicine of Ribeirão Preto. Department of Morphology. Ribeirão Preto, SP, SP, Brasi
dc.creator.affilliationUniversity of São Paulo. Institute of Biomedical Sciences-IV. Department of Immunology. São Paulo, SP, Brazil
dc.subject.enTrypanosoma cruzi
dc.subject.enInfection
dc.subject.enCells NK
dc.subject.enAnimals
dc.subject.enMice
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