Journal article icon

Journal article

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

Abstract:
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.
Publication status:
Published
Peer review status:
Peer reviewed

Actions


Access Document


Publisher copy:
10.1002/eji.201546252

Authors



Publisher:
Wiley
Journal:
European Journal of Immunology More from this journal
Volume:
46
Issue:
8
Pages:
1854-1866
Publication date:
2016-05-01
Acceptance date:
2016-05-12
DOI:
EISSN:
1521-4141
ISSN:
0014-2980
Pmid:
27198486


Language:
English
Keywords:
Pubs id:
pubs:809050
UUID:
uuid:5a369f70-5ac4-4bb4-8578-baff5637ff38
Local pid:
pubs:809050
Source identifiers:
809050
Deposit date:
2017-12-11

Terms of use



Views and Downloads






If you are the owner of this record, you can report an update to it here: Report update to this record

TO TOP