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Liver accumulation of Plasmodium chabaudi-infected red blood cells and modulation of regulatory T cell and dendritic cell responses

2013-11-27Journal article Open access
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dc.contributor.authorMedeiros, Márcia M
dc.contributor.authorda Silva, Henrique B
dc.contributor.authorReis, Aramys S
dc.contributor.authorBarboza, Renato
dc.contributor.authorThompson, Joanne
dc.contributor.authorLima, Maria Regina D'Império
dc.contributor.authorMarinho, Cláudio R F
dc.contributor.authorTadokoro, Carlos E
dc.date.accessioned2015-11-25T16:49:55Z
dc.date.available2015-11-25T16:49:55Z
dc.date.issued2013-11-27
dc.description.abstractIt is postulated that accumulation of malaria-infected Red Blood Cells (iRBCs) in the liver could be a parasitic escape mechanism against full destruction by the host immune system. Therefore, we evaluated the in vivo mechanism of this accumulation and its potential immunological consequences. A massive liver accumulation of P. c. chabaudi AS-iRBCs (Pc-iRBCs) was observed by intravital microscopy along with an over expression of ICAM-1 on day 7 of the infection, as measured by qRT-PCR. Phenotypic changes were also observed in regulatory T cells (Tregs) and dendritic cells (DCs) that were isolated from infected livers, which indicate a functional role for Tregs in the regulation of the liver inflammatory immune response. In fact, the suppressive function of liver-Tregs was in vitro tested, which demonstrated the capacity of these cells to suppress naive T cell activation to the same extent as that observed for spleen-Tregs. On the other hand, it is already known that CD4+ T cells isolated from spleens of protozoan parasite-infected mice are refractory to proliferate in vivo. In our experiments, we observed a similar lack of in vitro proliferative capacity in liver CD4+ T cells that were isolated on day 7 of infection. It is also known that nitric oxide and IL-10 are partially involved in acute phase immunosuppression; we found high expression levels of IL-10 and iNOS mRNA in day 7-infected livers, which indicates a possible role for these molecules in the observed immune suppression. Taken together, these results indicate that malaria parasite accumulation within the liver could be an escape mechanism to avoid sterile immunity sponsored by a tolerogenic environment.pt_PT
dc.description.sponsorshipCAPES-FCT travel grant: (#258/2010), CAPES-IGC grant: (#04/2012), Fundação de Apoio à Pesquisa do Estado de São Paulo – FAPESP grant: (#2009/53.889-0).pt_PT
dc.identifier.citationMedeiros MM, Silva HBd, Reis AS, Barboza R, Thompson J, et al. (2013) Liver Accumulation of Plasmodium chabaudi -Infected Red Blood Cells and Modulation of Regulatory T Cell and Dendritic Cell Responses. PLoS ONE 8(11): e81409. doi:10.1371/journal.pone.0081409pt_PT
dc.identifier.doi10.1371/journal.pone.0081409pt_PT
dc.identifier.urihttp://hdl.handle.net/10400.7/525
dc.language.isoengpt_PT
dc.peerreviewedyespt_PT
dc.publisherPLOSpt_PT
dc.relationGeneration of new transgenic animals for in vivo tracking of Regulatory T cells
dc.relation.publisherversionhttp://journals.plos.org/plosone/article?id=10.1371/journal.pone.0081409pt_PT
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/pt_PT
dc.subjectAnimalspt_PT
dc.subjectCell Proliferationpt_PT
dc.subjectDendritic Cellspt_PT
dc.subjectErythrocytespt_PT
dc.subjectFemalept_PT
dc.subjectLiverpt_PT
dc.subjectMicept_PT
dc.subjectPhenotypept_PT
dc.subjectPlasmodium chabaudipt_PT
dc.subjectT-Lymphocytes, Regulatorypt_PT
dc.titleLiver accumulation of Plasmodium chabaudi-infected red blood cells and modulation of regulatory T cell and dendritic cell responsespt_PT
dc.typejournal article
dspace.entity.typePublication
oaire.awardTitleGeneration of new transgenic animals for in vivo tracking of Regulatory T cells
oaire.awardURIinfo:eu-repo/grantAgreement/FCT/3599-PPCDT/PTDC%2FEBB-BIO%2F115514%2F2009/PT
oaire.citation.endPage15pt_PT
oaire.citation.issue11pt_PT
oaire.citation.startPage1pt_PT
oaire.citation.titlePLOS Onept_PT
oaire.citation.volume8pt_PT
oaire.fundingStream3599-PPCDT
project.funder.identifierhttp://doi.org/10.13039/501100001871
project.funder.nameFundação para a Ciência e a Tecnologia
rcaap.rightsopenAccesspt_PT
rcaap.typearticlept_PT
relation.isProjectOfPublication34ec30ee-f065-4b38-8a34-9c3c95346f02
relation.isProjectOfPublication.latestForDiscovery34ec30ee-f065-4b38-8a34-9c3c95346f02

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