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Apolipoproteins L control cell death triggered by TLR3/TRIF signaling in dendritic cells

Sophie Uzureau1, Caroline Coquerelle2, Corentin Vermeiren1

  • 1Laboratoire de Parasitologie Moléculaire, IBMM, Université Libre de Bruxelles, Gosselies, Belgium.

European Journal of Immunology
|May 21, 2016
PubMed

Insights

Viral stimuli, like poly(I:C), activate Toll-like receptor 3 (TLR3) signaling, inducing Apolipoproteins L (ApoLs) in dendritic cells (DCs). ApoLs promote DC death, suggesting a role in antiviral immune responses.

Area of Science:

  • Immunology
  • Cell Biology
  • Molecular Biology

Background:

  • Apolipoproteins L (ApoLs) are Bcl-2-like proteins.
  • ApoLs are expressed in myeloid and endothelial cells during inflammation.

Purpose of the Study:

  • To investigate the induction and function of ApoLs in dendritic cells (DCs) upon viral stimulation.
  • To explore the role of ApoLs in DC death and autophagy.

Main Methods:

  • Murine and human monocyte-derived DCs were treated with polyinosinic:polycytidylic acid (poly(I:C)), a Toll-like receptor (TLR) 3 agonist.
  • TLR3/TRIF signaling pathway and interferon-beta (IFN-β) dependency were analyzed.
  • ApoLs expression, cell death, and autophagy were assessed.
  • Knockdown of ApoLs was performed to evaluate its effect on DC survival.

Main Results:

  • Poly(I:C) specifically induced ApoLs7/11 subfamilies in murine CD8α(+) DCs via TLR3/TRIF/IFN-β signaling.
  • Poly(I:C) treatment induced both cell death and autophagy in DCs.
  • ApoLs expression correlated with poly(I:C)-induced DC death; ApoLs7/11 knockdown increased DC survival.
  • ApoLs7 associated with the anti-apoptotic protein Bcl-xL.
  • Human monocyte-derived DCs also showed poly(I:C)-induced cell death and ApoLs expression (principally ApoL3).
  • The BH3-like peptide of ApoLs was implicated in promoting DC death.

Conclusions:

  • ApoLs are involved in cell death pathways linked to DC activation by viral stimuli.
  • ApoLs may play a significant role in regulating immune cell fate during viral infections.
Keywords:
ApoL1Apolipoproteins LBcl-xLCell deathDendritic cells ⋅ Poly(I :C)TLR3TRIF

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