B16 melanoma cells increase B-1 cell survival, IL-10 production and radioresistance in vitro

Página do item simplificado
dc.contributor.authorLucatelli Laurindo, Maria Fernanda [UNIFESP]
dc.contributor.authorThies, Felipe Garutti [UNIFESP]
dc.contributor.authorPerez, Elizabeth Cristina [UNIFESP]
dc.contributor.authorNovaes e Brito, Ronni Romulo [UNIFESP]
dc.contributor.authorMariano, Mario [UNIFESP]
dc.contributor.authorPopi, Ana Flavia [UNIFESP]
dc.contributor.institutionUniversidade Federal de São Paulo (UNIFESP)
dc.contributor.institutionUniv Paulista UNIP
dc.date.accessioned2016-01-24T14:31:31Z
dc.date.available2016-01-24T14:31:31Z
dc.date.issued2013-04-01
dc.description.abstractB-1 cells can be differentiated from B-2 cells because they are predominantly located in the peritoneal and pleural cavities and have distinct phenotypic patterns and activation properties. the role of both cell populations in cancer progression is still controversial. Previous studies have indicated that direct contact between B-1 cells and B16 melanoma tumor cells (B16) increases the metastatic potential of the tumor cells. However, cellular changes that are induced in B-1 cells during the interaction between these two cell types have not been evaluated. in the present study, it is hypothesized that B-1 cells are modified after their interaction with tumor cells, leading to both increased cell viability and rate of proliferation. Additionally, soluble factors that were secreted by B16 cells were sufficient to augment B-1 cell viability and to modify the production of IL-10 by B-1 cells. Impressively, after direct or indirect contact with the B16 cells, B-1 cells became resistant to radiation-induced cell death. Thus, future studies that assess the importance of concomitant immunity and other conventional therapies in cancer treatment are needed. (C) 2012 Elsevier GmbH. All rights reserved.en
dc.description.affiliationUniversidade Federal de São Paulo, Dept Microbiol Immunol & Parasitol, Discipline Immunol, BR-04023900 São Paulo, Brazil
dc.description.affiliationUniv Paulista UNIP, São Paulo, Brazil
dc.description.affiliationUnifespUniversidade Federal de São Paulo, Dept Microbiol Immunol & Parasitol, Discipline Immunol, BR-04023900 São Paulo, Brazil
dc.description.sourceWeb of Science
dc.description.sponsorshipFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.description.sponsorshipConselho Nacional de Pesquisa
dc.description.sponsorshipCoordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
dc.description.sponsorshipIDFAPESP: 2008/58561-0
dc.description.sponsorshipIDConselho Nacional de Pesquisa: CNPq - 142676/07-1
dc.description.sponsorshipIDCAPES: 1326/09-0
dc.format.extent609-619
dc.identifierhttp://dx.doi.org/10.1016/j.imbio.2012.07.032
dc.identifier.citationImmunobiology. Jena: Elsevier Gmbh, Urban & Fischer Verlag, v. 218, n. 4, p. 609-619, 2013.
dc.identifier.doi10.1016/j.imbio.2012.07.032
dc.identifier.issn0171-2985
dc.identifier.urihttp://repositorio.unifesp.br/handle/11600/36160
dc.identifier.wosWOS:000319024100021
dc.language.isoeng
dc.publisherElsevier B.V.
dc.relation.ispartofImmunobiology
dc.rightsAcesso restrito
dc.rights.licensehttp://www.elsevier.com/about/open-access/open-access-policies/article-posting-policy
dc.subjectB-1 cellsen
dc.subjectB16 cellsen
dc.subjectIL-10en
dc.subjectRadioresistanceen
dc.titleB16 melanoma cells increase B-1 cell survival, IL-10 production and radioresistance in vitroen
dc.typeArtigo
Arquivos
Coleções
EPM - Artigos