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T cell biasing by activated dendritic cells.

Charles F Anderson1, Mark Lucas, Laila Gutiérrez-Kobeh

  • 1Department of Cell Biology and Molecular Genetics, University of Maryland, College Park, MD 20742, USA.

Journal of Immunology (Baltimore, Md. : 1950)
|July 9, 2004
PubMed
Summary
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Immune complexes alter dendritic cell (DC) cytokine production, shifting T cell responses from Th1 to Th2. This immune complex response by DCs prevents the typical Th1 bias seen in innate immune activation.

Area of Science:

  • Immunology
  • Cell Biology
  • Molecular Biology

Background:

  • Macrophages and dendritic cells (DCs) express Fc gamma receptors (FcgammaRs) and influence T cell activation.
  • Previous studies showed FcgammaR ligation affects macrophage cytokine production and T cell responses.

Purpose of the Study:

  • To investigate if dendritic cells (DCs) respond to immune complexes similarly to macrophages.
  • To determine how immune complexes impact DC cytokine production and subsequent T cell responses.

Main Methods:

  • Activation of murine dendritic cells (DCs) with and without immune complexes.
  • Analysis of DC cytokine production (IL-12p70).
  • Assessment of T cell cytokine responses (IFN-gamma, Th2-like).
  • DC transfer experiments and vaccination studies in mice.

Related Experiment Videos

  • Investigation of IL-12 gene expression (p40 and p35 subunits).

    • Main Results:

    • Activated DCs normally induce naive T cells to produce IFN-gamma (Th1 response).
    • DCs activated with immune complexes reduce IL-12p70 production and induce a Th2-like cytokine response.
    • DC transfer experiments showed immune complexes promote higher Ag-specific IgG1 antibody levels.
    • DCs down-regulate IL-12 p35 expression, unlike macrophages which down-regulate both p40 and p35.

    Conclusions:

    • Dendritic cells (DCs) alter their cytokine production in response to immune complexes, influencing T cell responses.
    • DCs expressing FcgammaRs can inhibit IL-12 biosynthesis upon encountering immune complexes.
    • This mechanism prevents the Th1-type T cell bias typically associated with innate immune activation.