Please use this identifier to cite or link to this item: https://repositorio.unifesp.br/handle/11600/29673
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dc.contributor.authorTzelepis, Fanny [UNIFESP]
dc.contributor.authorPersechini, Pedro M.
dc.contributor.authorRodrigues, Mauricio M. [UNIFESP]
dc.date.accessioned2016-01-24T13:48:36Z-
dc.date.available2016-01-24T13:48:36Z-
dc.date.issued2007-04-25
dc.identifierhttp://dx.doi.org/10.1371/journal.pone.0000393
dc.identifier.citationPlos One. San Francisco: Public Library Science, v. 2, n. 4, 9 p., 2007.
dc.identifier.issn1932-6203
dc.identifier.urihttp://repositorio.unifesp.br/handle/11600/29673-
dc.description.abstractBackground. Following infection with viruses, bacteria or protozoan parasites, naive antigen-specific CD8(+) T cells undergo a process of differentiation and proliferation to generate effector cells. Recent evidences suggest that the timing of generation of specific effector CD8(+) T cells varies widely according to different pathogens. We hypothesized that the timing of increase in the pathogen load could be a critical parameter governing this process. Methodology/Principal Findings. Using increasing doses of the protozoan parasite Trypanosoma cruzi to infect C57BL/6 mice, we observed a significant acceleration in the timing of parasitemia without an increase in mouse susceptibility. in contrast, in CD8 deficient mice, we observed an inverse relationship between the parasite inoculum and the timing of death. These results suggest that in normal mice CD8(+) T cells became protective earlier, following the accelerated development of parasitemia. the evaluation of specific cytotoxic responses in vivo to three distinct epitopes revealed that increasing the parasite inoculum hastened the expansion of specific CD8(+) cytotoxic T cells following infection. the differentiation and expansion of T. cruzi-specific CD8(+) cytotoxic T cells is in fact dependent on parasite multiplication, as radiation-attenuated parasites were unable to activate these cells. We also observed that, in contrast to most pathogens, the activation process of T. cruzi-specific CD8(+) cytotoxic T cells was dependent on MHC class II restricted CD4(+) T cells. Conclusions/Significance. Our results are compatible with our initial hypothesis that the timing of increase in the pathogen load can be a critical parameter governing the kinetics of CD4(+) T cell-dependent expansion of pathogen-specific CD8(+) cytotoxic T cells.en
dc.description.sponsorshipFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.description.sponsorshipMillennium Institute for Vaccine Development and Technology
dc.description.sponsorshipConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
dc.format.extent9
dc.language.isoeng
dc.publisherPublic Library Science
dc.relation.ispartofPlos One
dc.rightsAcesso aberto
dc.titleModulation of CD4(+) T Cell-Dependent Specific Cytotoxic CD8(+) T Cells Differentiation and Proliferation by the Timing of Increase in the Pathogen Loaden
dc.typeArtigo
dc.contributor.institutionUniversidade Federal de São Paulo (UNIFESP)
dc.contributor.institutionUniversidade Federal do Rio de Janeiro (UFRJ)
dc.description.affiliationUniversidade Federal de São Paulo, Escola Paulista Med, CINTERGEN, São Paulo, Brazil
dc.description.affiliationUniversidade Federal de São Paulo, Escola Paulista Med, Dept Microbiol Imunol & Parasitol, São Paulo, Brazil
dc.description.affiliationUniv Fed Rio de Janeiro, Inst Biofis Carlos Chagas Filho, Ilha Fundao, Ctr Ciencias Saude, BR-21941 Rio de Janeiro, Brazil
dc.description.affiliationUnifespUniversidade Federal de São Paulo, Escola Paulista Med, CINTERGEN, São Paulo, Brazil
dc.description.affiliationUnifespUniversidade Federal de São Paulo, Escola Paulista Med, Dept Microbiol Imunol & Parasitol, São Paulo, Brazil
dc.description.sponsorshipIDMillennium Institute for Vaccine Development and Technology: CNPq - 420067/2005-1
dc.identifier.fileWOS000207445600007.pdf
dc.identifier.doi10.1371/journal.pone.0000393
dc.description.sourceWeb of Science
dc.identifier.wosWOS:000207445600007
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