Please use this identifier to cite or link to this item: https://repositorio.unifesp.br/handle/11600/44423
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dc.contributor.authorTzelepis, Fanny [UNIFESP]
dc.contributor.authorAlencar, Bruna C. G. de [UNIFESP]
dc.contributor.authorPenido, Marcus L. O.
dc.contributor.authorClaser, Carla [UNIFESP]
dc.contributor.authorMachado, Alexandre V.
dc.contributor.authorBruna-Romero, Oscar
dc.contributor.authorGazzinelli, Ricardo T.
dc.contributor.authorRodrigues, Mauricio M. [UNIFESP]
dc.date.accessioned2018-06-15T18:02:28Z-
dc.date.available2018-06-15T18:02:28Z-
dc.date.issued2008-02-01
dc.identifierhttp://dx.doi.org/10.4049/jimmunol.180.3.1737
dc.identifier.citationJournal Of Immunology. Bethesda: Amer Assoc Immunologists, v. 180, n. 3, p. 1737-1748, 2008.
dc.identifier.issn0022-1767
dc.identifier.urihttp://repositorio.unifesp.br/11600/44423-
dc.description.abstractInterference or competition between CD8(+) T cells restricted by distinct MHC-I molecules can be a powerful means to establish an immunodominant response. However, its importance during infections is still questionable. In this study, we describe that following infection of mice with the human pathogen Trypanosoma cruzi, an immunodominant CD8(+) T cell immune response is developed directed to an H-2K(b)-restricted epitope expressed by members of the trans-sialidase family of surface proteins. To determine whether this immunodominance was exerted over other non-H-2K(b)-restricted epitopes, we measured during infection of heterozygote mice, immune responses to three distinct epitopes, all expressed by members of the trans-sialidase family, recognized by H-2k(b)-, H-2K(k)-, or H-2K(d)-restricted CD8(+) T cells. Infected heterozygote or homozygote mice displayed comparably strong immune responses to the H-2k(b)-restricted immunodominant epitope. In contrast, 11-2K(k) or H-2K(d)-restricted immune responses were significantly impaired in heterozygote infected mice when compared with homozygote ones. This interference was not dependent on the dose of parasite or the timing of infection. Also, it was not seen in heterozygote mice immunized with recombinant adenoviruses expressing T. cruzi Ags. Finally, we observed that the immunodominance was circumvented by concomitant infection with two T. cruzi strains containing distinct immunodominant epitopes, suggesting that the operating mechanism most likely involves competition of T cells for limiting APCs. This type of interference never described during infection with a human parasite may represent a sophisticated strategy to restrict priming of CD8(+) T cells of distinct specificities, avoiding complete pathogen elimination by host effector cells, and thus favoring host parasitism.en
dc.format.extent1737-1748
dc.language.isoeng
dc.publisherAmer Assoc Immunologists
dc.relation.ispartofJournal Of Immunology
dc.rightsAcesso restrito
dc.titleInfection with Trypanosoma cruzi restricts the repertoire of parasite-specific CD8(+) T cells leading to immunodominanceen
dc.typeArtigo
dc.contributor.institutionUniversidade Federal de São Paulo (UNIFESP)
dc.contributor.institutionUniversidade Federal de Minas Gerais (UFMG)
dc.contributor.institutionFundacao Oswaldo Cruz
dc.description.affiliationUniv Fed Sao Paulo, Escola Paulista Med, Ctr Interdisciplinar Terapia Gen, BR-04044010 Sao Paulo, Brazil
dc.description.affiliationUniv Fed Sao Paulo, Escola Paulista Med, Dept Microbiol Imunol & Parasitol, BR-04044010 Sao Paulo, Brazil
dc.description.affiliationUniv Fed Minas Gerais, Inst Ciencias Biol, Dept Bioquim & Imunol, Belo Horizonte, MG, Brazil
dc.description.affiliationUniv Fed Minas Gerais, Inst Ciencias Biol, Dept Microbiol, Belo Horizonte, MG, Brazil
dc.description.affiliationFundacao Oswaldo Cruz, Ctr Pesquisas Rene Rachou, Belo Horizonte, MG, Brazil
dc.description.affiliationUnifespUniv Fed Sao Paulo, Escola Paulista Med, Ctr Interdisciplinar Terapia Gen, BR-04044010 Sao Paulo, Brazil
dc.description.affiliationUnifespUniv Fed Sao Paulo, Escola Paulista Med, Dept Microbiol Imunol & Parasitol, BR-04044010 Sao Paulo, Brazil
dc.identifier.doi10.4049/jimmunol.180.3.1737
dc.description.sourceWeb of Science
dc.identifier.wosWOS:000252632900050
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Artigo

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