| First Author | Uzureau S | Year | 2016 |
| Journal | Eur J Immunol | Volume | 46 |
| Issue | 8 | Pages | 1854-66 |
| PubMed ID | 27198486 | Mgi Jnum | J:249795 |
| Mgi Id | MGI:5923265 | Doi | 10.1002/eji.201546252 |
| Citation | Uzureau S, et al. (2016) Apolipoproteins L control cell death triggered by TLR3/TRIF signaling in dendritic cells. Eur J Immunol 46(8):1854-66 |
| abstractText | 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 CD8alpha(+) dendritic cells (DCs). This induction requires the TLR3/TRIF (where TRIF is TIR domain containing adapter-inducing interferon beta) signaling pathway and is dependent on IFN-beta 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. |
