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10.1016/j.cell.2017.09.039 http://scihub22266oqcxt.onion/10.1016/j.cell.2017.09.039 C5901709!5901709 !29033128     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=29033128 &cmd=llinks): Failed to open stream: HTTP request failed! 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The DNA Inflammasome in Human Myeloid Cells Is Initiated by a STING-Cell Death Program Upstream of NLRP3 |pdf=|usr=}}{{29033128 }} gab.com Text The DNA Inflammasome in Human Myeloid Cells Is Initiated by a STING-Cell Death Program Upstream of NLRP3 JO: Cell http://www.kidney.de/pget.php?&tw=1&pmid=29033128 #FOAvip Detection of cytosolic DNA constitutes a central event in the context of numerous infectious and sterile inflammatory conditions. Recent studies have uncovered a bipartite mode of cytosolic DNA recognition, in which the cGAS-STING axis triggers antiviral immunity, whereas AIM2 triggers inflammasome activation. Here, we show that AIM2 is dispensable for DNA-mediated inflammasome activation in human myeloid cells. Instead, detection of cytosolic DNA by the cGAS-STING axis induces a cell death program initiating potassium efflux upstream of NLRP3. Forward genetics identified regulators of lysosomal trafficking to modulate this cell death program, and subsequent studies revealed that activated STING traffics to the lysosome, where it triggers membrane permeabilization and thus lysosomal cell death (LCD). Importantly, the cGAS-STING-NLRP3 pathway constitutes the default inflammasome response during viral and bacterial infections in human myeloid cells. We conclude that targeting the cGAS-STING-LCD-NLRP3 pathway will ameliorate pathology in inflammatory conditions that are associated with cytosolic DNA sensing. Twit Text FOAVip The DNA Inflammasome in Human Myeloid Cells Is Initiated by a STING-Cell Death Program Upstream of NLRP3 ????Cell http://www.kidney.de/pget.php?&tw=1&pmid=29033128 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29033128 #FOAvip English Wikipedia <ref>{{Cite pmid|29033128 }}</ref> The DNA Inflammasome in Human Myeloid Cells Is Initiated by a STING-Cell Death Program Upstream of NLRP3 #MMPMID29033128 Gaidt MM ; Ebert TS ; Chauhan D ; Ramshorn K ; Pinci F ; Zuber S ; O'Duill F ; Schmid-Burgk JL ; Hoss F ; Buhmann R ; Wittmann G ; Latz E ; Subklewe M ; Hornung V Cell 2017[Nov]; 171 (5 ): 1110-1124.e18 PMID29033128 show ga Detection of cytosolic DNA constitutes a central event in the context of numerous infectious and sterile inflammatory conditions. Recent studies have uncovered a bipartite mode of cytosolic DNA recognition, in which the cGAS-STING axis triggers antiviral immunity, whereas AIM2 triggers inflammasome activation. Here, we show that AIM2 is dispensable for DNA-mediated inflammasome activation in human myeloid cells. Instead, detection of cytosolic DNA by the cGAS-STING axis induces a cell death program initiating potassium efflux upstream of NLRP3. Forward genetics identified regulators of lysosomal trafficking to modulate this cell death program, and subsequent studies revealed that activated STING traffics to the lysosome, where it triggers membrane permeabilization and thus lysosomal cell death (LCD). Importantly, the cGAS-STING-NLRP3 pathway constitutes the default inflammasome response during viral and bacterial infections in human myeloid cells. We conclude that targeting the cGAS-STING-LCD-NLRP3 pathway will ameliorate pathology in inflammatory conditions that are associated with cytosolic DNA sensing. |*Cell Death [MESH] |DNA/metabolism [MESH] |Humans [MESH] |Inflammasomes/*metabolism [MESH] |Membrane Proteins/metabolism [MESH] |Monocytes/*cytology/metabolism [MESH] |NLR Family, Pyrin Domain-Containing 3 Protein/*metabolism [MESH]The DNA Inflammasome in Human Myeloid Cells Is Initiated by a STING-Ce(epmc).pdf DeepDyve Pubget Overpricing