Human Dendritic Cells Produce TGF-β1 under the Influence of Lung Carcinoma Cells and Prime the Differentiation of CD4+CD25+Foxp3+ Regulatory T Cells

DOI PDF 被引用文献4件
  • Ingrid E Dumitriu
    Centre for Inflammation Research, Queen’s Medical Research Institute, University of Edinburgh , Edinburgh,
  • Donald R Dunbar
    Centre for Inflammation Research, Queen’s Medical Research Institute, University of Edinburgh , Edinburgh,
  • Sarah E Howie
    Centre for Inflammation Research, Queen’s Medical Research Institute, University of Edinburgh , Edinburgh,
  • Tariq Sethi
    Centre for Inflammation Research, Queen’s Medical Research Institute, University of Edinburgh , Edinburgh,
  • Christopher D Gregory
    Centre for Inflammation Research, Queen’s Medical Research Institute, University of Edinburgh , Edinburgh,

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公開日
2009-03-01
権利情報
  • https://academic.oup.com/pages/standard-publication-reuse-rights
DOI
  • 10.4049/jimmunol.0712671
公開者
Oxford University Press (OUP)

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<jats:title>Abstract</jats:title> <jats:p>Dendritic cells (DCs) have a central role in the development of adaptive immune responses, including antitumor immunity. Factors present in the tumor milieu can alter the maturation of DCs and inhibit their capacity to activate T cells. Using gene expression analysis, we found that human DCs increased the expression of TGF-β1 transcripts following culture with human lung carcinoma cells (LCCs). These DCs produced increased amounts of TGF-β1 protein compared with DCs not exposed to tumor cells. LCCs also decreased the expression of CD86 and HLA-DR by immature DCs. Furthermore, LCCs decreased CD86 expression and the production of TNF-α and IL-12 p70 by mature DCs. Moreover, LCCs also converted mature DCs into cells producing TGF-β1. These TGF-β1-producing DCs were poor at eliciting the activation of naive CD4+ T cells and sustaining their proliferation and differentiation into Th1 (IFN-γ+) effectors. Instead, TGF-β1-producing DCs demonstrated an increased ability to generate CD4+CD25+Foxp3+ regulatory T cells that suppress the proliferation of T lymphocytes. These results identify a novel mechanism by which the function of human DCs is altered by tumor cells and contributes to the evasion of the immune response.</jats:p>

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