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

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

Autor Lucatelli Laurindo, Maria Fernanda Autor UNIFESP Google Scholar
Thies, Felipe Garutti Autor UNIFESP Google Scholar
Perez, Elizabeth Cristina Autor UNIFESP Google Scholar
Novaes e Brito, Ronni Romulo Autor UNIFESP Google Scholar
Mariano, Mario Autor UNIFESP Google Scholar
Popi, Ana Flavia Autor UNIFESP Google Scholar
Instituição Universidade Federal de São Paulo (UNIFESP)
Univ Paulista UNIP
Resumo B-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.
Palavra-chave B-1 cells
B16 cells
IL-10
Radioresistance
Idioma Inglês
Financiador Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
Conselho Nacional de Pesquisa
Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
Número do financiamento FAPESP: 2008/58561-0
Conselho Nacional de Pesquisa: CNPq - 142676/07-1
CAPES: 1326/09-0
Data de publicação 2013-04-01
Publicado em Immunobiology. Jena: Elsevier Gmbh, Urban & Fischer Verlag, v. 218, n. 4, p. 609-619, 2013.
ISSN 0171-2985 (Sherpa/Romeo, fator de impacto)
Publicador Elsevier B.V.
Extensão 609-619
Fonte http://dx.doi.org/10.1016/j.imbio.2012.07.032
Direito de acesso Acesso restrito
Tipo Artigo
Web of Science WOS:000319024100021
Endereço permanente http://repositorio.unifesp.br/handle/11600/36160

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