Tumor necrosis factor-α promotes survival and phenotypic maturation of poly(I:C)-treated dendritic cells but impairs their Th1 and Th17 polarizing capability

Cytotherapy. 2015 May;17(5):633-46. doi: 10.1016/j.jcyt.2014.11.006. Epub 2015 Jan 2.

Abstract

Background aims: Toll-like receptor (TLR)-3 synthetic agonist polyinosinic-polycytidylic acid (poly(I:C)) is a promising agent for dendritic cell (DC)-based anti-tumor vaccines because of its ability to induce a strong maturation of DCs, but such an effect is followed by stimulation of DC apoptosis. Tumor necrosis factor (TNF)-α may promote the survival of poly(I:C)-stimulated DCs, but it is not known in detail how this combination affects the maturation and polarization capacity of monocyte-derived (Mo)DCs.

Methods: Immature MoDCs, generated from human monocytes, were treated with different concentrations of poly(I:C) combined with TNF-α, and the effect on survival, phenotype, production of cytokines, allostimulatory and Th polarization capacity was assessed after 24 and 48 h.

Results: We showed that TNF-α inhibited the dose-dependent pro-apoptotic effect of poly(I:C). However, TNF-α also decreased poly(I:C)-induced production of interleukin (IL)-12 and IL-23 by MoDCs, which correlated with their diminished capacity to stimulate cellular proliferation, interferon-γ and IL-17 production by allogeneic CD4(+)T cells in co-culture. Such an effect was more pronounced after 24 h and could not be restored by CD40 ligation. In the presence of CD40L, TNF-α even stimulated IL-10 production and immunoglobulin-like transcript 3 expression by poly(I:C)-matured DCs, which correlated with their increased capacity to induce IL-10 production by CD4(+)T cells.

Conclusion: Even though TNF-α could promote the survival of poly(I:C)-matured MoDCs, it also suppresses key anti-tumor functions of these cells, which could have important implications when considering this, already suggested, protocol for the DC-based anti-tumor therapy.

Keywords: DC-based tumor vaccines; TNF-α; Th-polarization; cytokines; dendritic cells; poly(I:C).

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Apoptosis / drug effects
  • CD40 Antigens / metabolism
  • CD40 Ligand / metabolism
  • Cell Differentiation / drug effects*
  • Cell Polarity / drug effects*
  • Cell Survival / drug effects
  • Coculture Techniques
  • Dendritic Cells / cytology*
  • Dendritic Cells / drug effects
  • Humans
  • Membrane Glycoproteins
  • Monocytes / cytology
  • Phenotype
  • Poly I-C / pharmacology*
  • Receptors, Cell Surface / metabolism
  • Receptors, Immunologic
  • Th1 Cells / cytology*
  • Th1 Cells / drug effects
  • Th17 Cells / cytology*
  • Th17 Cells / drug effects
  • Th17 Cells / metabolism
  • Tumor Necrosis Factor-alpha / pharmacology*

Substances

  • CD40 Antigens
  • LILRB4 protein, human
  • Membrane Glycoproteins
  • Receptors, Cell Surface
  • Receptors, Immunologic
  • TNF protein, human
  • Tumor Necrosis Factor-alpha
  • CD40 Ligand
  • Poly I-C