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10.1084/jem.20151876 http://scihub22266oqcxt.onion/10.1084/jem.20151876 C4854735!4854735 !27091841     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27091841 &cmd=llinks): Failed to open stream: HTTP request failed! 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Oxidized mitochondrial nucleoids released by neutrophils drive type I interferon production in human lupus |pdf=|usr=}}{{27091841 }} gab.com Text Oxidized mitochondrial nucleoids released by neutrophils drive type I interferon production in human lupus JO: J Exp Med http://www.kidney.de/pget.php?&tw=1&pmid=27091841 #FOAvip Autoantibodies against nucleic acids and excessive type I interferon (IFN) are hallmarks of human systemic lupus erythematosus (SLE). We previously reported that SLE neutrophils exposed to TLR7 agonist autoantibodies release interferogenic DNA, which we now demonstrate to be of mitochondrial origin. We further show that healthy human neutrophils do not complete mitophagy upon induction of mitochondrial damage. Rather, they extrude mitochondrial components, including DNA (mtDNA), devoid of oxidized (Ox) residues. When mtDNA undergoes oxidation, it is directly routed to lysosomes for degradation. This rerouting requires dissociation from the transcription factor A mitochondria (TFAM), a dual high-mobility group (HMG) protein involved in maintenance and compaction of the mitochondrial genome into nucleoids. Exposure of SLE neutrophils, or healthy IFN-primed neutrophils, to antiribonucleotide protein autoantibodies blocks TFAM phosphorylation, a necessary step for nucleoid dissociation. Consequently, Ox nucleoids accumulate within mitochondria and are eventually extruded as potent interferogenic complexes. In support of the in vivo relevance of this phenomenon, mitochondrial retention of Ox nucleoids is a feature of SLE blood neutrophils, and autoantibodies against Ox mtDNA are present in a fraction of patients. This pathway represents a novel therapeutic target in human SLE. Twit Text FOAVip Oxidized mitochondrial nucleoids released by neutrophils drive type I interferon production in human lupus ????J Exp Med http://www.kidney.de/pget.php?&tw=1&pmid=27091841 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27091841 #FOAvip English Wikipedia <ref>{{Cite pmid|27091841 }}</ref> Oxidized mitochondrial nucleoids released by neutrophils drive type I interferon production in human lupus #MMPMID27091841 Caielli S ; Athale S ; Domic B ; Murat E ; Chandra M ; Banchereau R ; Baisch J ; Phelps K ; Clayton S ; Gong M ; Wright T ; Punaro M ; Palucka K ; Guiducci C ; Banchereau J ; Pascual V J Exp Med 2016[May]; 213 (5 ): 697-713 PMID27091841 show ga Autoantibodies against nucleic acids and excessive type I interferon (IFN) are hallmarks of human systemic lupus erythematosus (SLE). We previously reported that SLE neutrophils exposed to TLR7 agonist autoantibodies release interferogenic DNA, which we now demonstrate to be of mitochondrial origin. We further show that healthy human neutrophils do not complete mitophagy upon induction of mitochondrial damage. Rather, they extrude mitochondrial components, including DNA (mtDNA), devoid of oxidized (Ox) residues. When mtDNA undergoes oxidation, it is directly routed to lysosomes for degradation. This rerouting requires dissociation from the transcription factor A mitochondria (TFAM), a dual high-mobility group (HMG) protein involved in maintenance and compaction of the mitochondrial genome into nucleoids. Exposure of SLE neutrophils, or healthy IFN-primed neutrophils, to antiribonucleotide protein autoantibodies blocks TFAM phosphorylation, a necessary step for nucleoid dissociation. Consequently, Ox nucleoids accumulate within mitochondria and are eventually extruded as potent interferogenic complexes. In support of the in vivo relevance of this phenomenon, mitochondrial retention of Ox nucleoids is a feature of SLE blood neutrophils, and autoantibodies against Ox mtDNA are present in a fraction of patients. This pathway represents a novel therapeutic target in human SLE. |Adolescent [MESH] |Autoantibodies/immunology [MESH] |Child [MESH] |Child, Preschool [MESH] |DNA, Mitochondrial/*immunology [MESH] |DNA-Binding Proteins/immunology [MESH] |Female [MESH] |Humans [MESH] |Interferon Type I/*immunology [MESH] |Lupus Erythematosus, Systemic/*immunology/pathology [MESH] |Male [MESH] |Mitochondria/*immunology/pathology [MESH] |Mitochondrial Proteins/immunology [MESH] |Neutrophils/*immunology/pathology [MESH] |Oxidation-Reduction [MESH] |Toll-Like Receptor 7/immunology [MESH]Oxidized mitochondrial nucleoids released by neutrophils drive type I (epmc).pdf DeepDyve Pubget Overpricing