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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


Eur J Immunol




1854 - 1866


ApoL1, Apolipoproteins L, Bcl-xL, Cell death, Dendritic cells ⋅ Poly(I :C), TLR3, TRIF, Adaptor Proteins, Vesicular Transport, Animals, Apolipoproteins, Apoptosis, CD8 Antigens, Cell Line, Cells, Cultured, Dendritic Cells, Humans, Interferon-beta, Mice, Mice, Inbred C57BL, Mice, Knockout, Poly I-C, Protein Isoforms, Signal Transduction, Toll-Like Receptor 3, bcl-X Protein