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

par Uzureau, Sophie ;Coquerelle, Caroline ;Vermeiren, Corentin ;Uzureau, Pierrick ;Van Acker, Annette;Pilotte, Luc;Monteyne, Daniel ;Acolty, Valérie ;Vanhollebeke, Benoît ;Van den Eynde, Benoît J;Perez-Morga, David ;Moser, Muriel ;Pays, Etienne
Référence European Journal of Immunology
Publication Publié, 2016-05

Article révisé par les pairs

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Résumé :

Apolipoproteins L (ApoLs) are Bcl-2-like proteins expressed under inflammatory conditions in myeloid and endothelial cells. We found that Toll-like receptor (TLR) stimuli, particularly the viral mimetic poly(I:C), specifically induce ApoLs7/11 sub-families in murine CD8α(+)  dendritic cells (DCs). This induction requires the TLR3/TRIF signaling pathway and is dependent on IFN-β in all ApoLs sub-families except for ApoL7c. Poly(I:C) treatment of DCs is also associated with induction of both cell death and autophagy. ApoLs expression is related to promotion of DC death by poly(I:C), as ApoLs7/11 knock-down increases DC survival and ApoLs7 are associated with the anti-apoptotic protein Bcl-xL. Similarly, in human monocyte-derived DCs poly(I:C) induces both cell death and the expression of ApoLs, principally ApoL3. Finally, the BH3-like peptide of ApoLs appears to be involved in the DC death-promoting activity. We would like to propose that ApoLs are involved in cell death linked to activation of DCs by viral stimuli. This article is protected by copyright. All rights reserved.