A Influência de Células B-1 na atividade supressora de células Treg FOXP3+ geradas in vitro

Detalhes bibliográficos
Ano de defesa: 2017
Autor(a) principal: Lima, Karina Alcantara de [UNIFESP]
Orientador(a): Não Informado pela instituição
Banca de defesa: Não Informado pela instituição
Tipo de documento: Dissertação
Tipo de acesso: Acesso aberto
Idioma: por
Instituição de defesa: Universidade Federal de São Paulo
Programa de Pós-Graduação: Não Informado pela instituição
Departamento: Não Informado pela instituição
País: Não Informado pela instituição
Palavras-chave em Português:
Link de acesso: https://sucupira.capes.gov.br/sucupira/public/consultas/coleta/trabalhoConclusao/viewTrabalhoConclusao.jsf?popup=true&id_trabalho=5454503
http://repositorio.unifesp.br/handle/11600/50688
Resumo: The role of B-1 cells in the development of Treg cells has been studied recently. In vitro assays demonstrated that B-1a cells are capable of converting CD4+CD25+ T cells into a cell with regulatory potential without FOXP3 expression. Previously, we demonstrated that B-1 cells could regulate the proliferative activity of FOXP3+ Treg cells in vitro e upregulate Treg cells population in the peritoneal cavity of mice, under physiological and pathogenic conditions. In this study, we aimed to understand the role of B-1 cells in the suppressive activity of FOXP3+ Treg cells generated in vitro with TGF-β stimulation. For this, we performed a co-culture of naive T-cell in the presence of B-1 cells, in order to generate in vitro Treg cells and, after, to evaluate the suppression mechanisms of these cells by effector T cell suppression assay. Thus, in vitro generation of Treg cells is more efficient in cocultures with B-1 cells, which favors the proliferation of Treg cells and modulate the cytokine profile into these cultures. These cells (called iTreg(B-1)) demonstrated suppressive activity similar to the observed in iTregs generated without B-1 cells and also natural Tregs. And we have also shown that B-1 cells can modify the mechanism of suppression in iTreg(B-1) increasing the relative gene expression of CTLA-4. Our results may contribute to future studies aimed therapy with Treg cells and new methodologies for obtaining such cells.