Cross Talk between Peritoneal Macrophages and B-1 Cells in Vitro

Cross Talk between Peritoneal Macrophages and B-1 Cells in Vitro

Author Thies, Felipe Garutti Autor UNIFESP Google Scholar
Laurindo, Maria Fernanda Lucatelli 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
Institution Universidade Federal de São Paulo (UNIFESP)
Univ Paulista UNIP
Abstract B-1 cells constitute a distinct B cell population with unique phenotypic and functional characteristics. They represent the main B cell population found in mouse peritoneal and pleural cavities. the communication between B-1 cells and peritoneal macrophages has been previously studied, and the effect this interaction has on macrophages has been previously described. Using an in vitro co-culture model, herein we demonstrated that peritoneal macrophages were able to increase survival rates and to stimulate proliferation of B-1 cells. IL-6 was also found to be important in B-1 cell survival; recombinant IL-6 increases the percentage of viable B-1 cells in culture. Furthermore, molecules involved in the IL-6 signaling pathway, such as STAT-3 and Bcl-2, were highly expressed in B-1 cells after co-culture with peritoneal macrophages. IL-6-deficient peritoneal macrophages were not able to increase B-1 cell survival, confirming the importance of this cytokine. Altogether, our results indicate a novel mechanism in which peritoneal macrophages are able to regulate the B-1 population via IL-6 secretion.
Language English
Sponsor Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
Grant number FAPESP: 2008/58561-0
FAPESP: 2011/50256-6
Date 2013-05-08
Published in Plos One. San Francisco: Public Library Science, v. 8, n. 5, 11 p., 2013.
ISSN 1932-6203 (Sherpa/Romeo, impact factor)
Publisher Public Library Science
Extent 11
Access rights Open access Open Access
Type Article
Web of Science ID WOS:000319055600045

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