skip to main content
Idioma:

Role of endogenous IFN- gamma in macrophage programming induced by IL-12 and IL-18

Karina R B Bastos Renato Barboza; Luiz Sardinha; Momtchilo Russo; José Maria Alvarez; Maria Regina D'Império Lima; Meeting of the Brazilian Society for Immunology (31. 2006 Búzios)

Abstracts São Paulo, SP: Brazilian Society for Immunology, 2006

São Paulo 2006

Item não circula. Consulte sua biblioteca.(Acessar)

  • Título:
    Role of endogenous IFN- gamma in macrophage programming induced by IL-12 and IL-18
  • Autor: Karina R B Bastos
  • Renato Barboza; Luiz Sardinha; Momtchilo Russo; José Maria Alvarez; Maria Regina D'Império Lima; Meeting of the Brazilian Society for Immunology (31. 2006 Búzios)
  • Assuntos: IMUNOLOGIA
  • É parte de: Abstracts São Paulo, SP: Brazilian Society for Immunology, 2006
  • Notas: Disponível em CD-ROM
  • Descrição: Introduction and objectives: It is well established that IL-12, in synergism with IL-18, is a potent stimulus for IFN-g production by NK, T and B cells. Yet, the effects of these cytokines on macrophages are largely unknown. Here, we investigated the role of IL-12/IL-18 on nitric oxide (NO) and TNF-a production by CD11b+ adherent peritoneal cells, focusing on the involvement of endogenously produced IFN-g. Methods and results: Cells from C57BL/6 mice released substantial amounts of NO when stimulated with IFN-g or LPS, but failed to respond to IL-12 and/or IL-18. However, IL-12/IL-18 pretreatment was able to program C57BL/6 cells to release 6-8 folds more NO and TNF-a in response to LPS or Trypanosoma cruzi stimulation, with NO levels directly correlating with macrophage resistance to intracellular parasite growth. Analysis of IL-12/IL-18-primed cells from knockout mice revealed that endogenous IFN-g, IFN-gR and IRF-1 were essential for LPS-induced NO release, but TNF-a production was IFN-gindependent. Conversely, the MyD88-dependent pathway was indispensable for IL-12/IL-18- programmed LPS-induced TNF-a production, but not for NO release. Contaminant T and NK cells largely modulated the IL-12/IL-18 programming of LPS-induced NO response through IFNg secretion. Nevertheless, a small population of IFN-g+ cells with a macrophage phenotype was also identified, particularly in the peritoneum of chronically T. cruzi-infected mice, reinforcing the
    notion that macrophages can be an alternative source of IFN-g. Conclusion: Taken together, our data contribute to elucidate the molecular basis of the IL-12/IL-18 autocrine pathway of macrophage activation, showing that endogenous IFN-g plays an important role in programming the NO response, whereas the TNF-a response occurs through an IFN-g-independent pathway.
  • Editor: São Paulo
  • Data de criação/publicação: 2006
  • Formato: res. IN.007.
  • Idioma: Inglês
Links
Voltar para lista de resultados

  • Realização: ABCD-USP USP   Logos de Redes Sociais: Freepik

Buscando em bases de dados remotas. Favor aguardar.