| Literature DB >> 28459443 |
Simon J Tavernier1,2,3, Fabiola Osorio1,2,3, Lana Vandersarren1,2,3, Jessica Vetters1,2,3, Nele Vanlangenakker1,2,3, Gert Van Isterdael1,2,4, Karl Vergote1,2,3, Riet De Rycke4,5, Eef Parthoens4,5, Lianne van de Laar1,3,6, Takao Iwawaki7, Juan R Del Valle8, Chih-Chi Andrew Hu9, Bart N Lambrecht1,2,3,10, Sophie Janssens1,2,3.
Abstract
The IRE1-XBP1 signalling pathway is part of a cellular programme that protects against endoplasmic reticulum (ER) stress, but also controls development and survival of immune cells. Loss of XBP1 in splenic type 1 conventional dendritic cells (cDC1s) results in functional alterations without affecting cell survival. However, in mucosal cDC1s, loss of XBP1 impaired survival in a tissue-specific manner-while lung cDC1s die, intestinal cDC1s survive. This was not caused by differential activation of ER stress cell-death regulators CHOP or JNK. Rather, survival of intestinal cDC1s was associated with their ability to shut down protein synthesis through a protective integrated stress response and their marked increase in regulated IRE1-dependent messenger RNA decay. Furthermore, loss of IRE1 endonuclease on top of XBP1 led to cDC1 loss in the intestine. Thus, mucosal DCs differentially mount ATF4- and IRE1-dependent adaptive mechanisms to survive in the face of ER stress.Entities:
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Year: 2017 PMID： 28459443 PMCID： PMC5563826 DOI： 10.1038/ncb3518
Source DB: PubMed Journal: Nat Cell Biol ISSN： 1465-7392 Impact factor: 28.824