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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 polyinosinic:polycytidylic acid (poly(I:C)), specifically induce ApoLs7/11 subfamilies in murine CD8α(+)  dendritic cells (DCs). This induction requires the TLR3/TRIF (where TRIF is TIR domain containing adapter-inducing interferon β) signaling pathway and is dependent on IFN-β in all ApoLs subfamilies 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 knockdown increases DC survival and ApoLs7 are associated with the anti-apoptotic protein Bcl-xL (where Bcl-xL is B-cell lymphoma extra large). 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.

Original publication




Journal article


European journal of immunology

Publication Date





1854 - 1866


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


Dendritic Cells, Cells, Cultured, Cell Line, Animals, Mice, Inbred C57BL, Mice, Knockout, Humans, Mice, Apolipoproteins, Interferon-beta, Adaptor Proteins, Vesicular Transport, Protein Isoforms, Poly I-C, Signal Transduction, Apoptosis, bcl-X Protein, Toll-Like Receptor 3, CD8 Antigens