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10.1002/art.39247 http://scihub22266oqcxt.onion/10.1002/art.39247 C4626310!4626310 !26097119     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26097119 &cmd=llinks): Failed to open stream: HTTP request failed! 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Release of neutrophil extracellular traps by neutrophils stimulated with antiphospholipid antibodies: a newly identified mechanism of thrombosis in the antiphospholipid syndrome |pdf=|usr=}}{{26097119 }} gab.com Text Release of neutrophil extracellular traps by neutrophils stimulated with antiphospholipid antibodies: a newly identified mechanism of thrombosis in the antiphospholipid syndrome JO: Arthritis Rheumatol http://www.kidney.de/pget.php?&tw=1&pmid=26097119 #FOAvip OBJECTIVE: Antiphospholipid antibodies (aPL), especially those targeting ?2 -glycoprotein I (?2 GPI), are well known to activate endothelial cells, monocytes, and platelets, with prothrombotic implications. In contrast, the interaction of aPL with neutrophils has not been extensively studied. Neutrophil extracellular traps (NETs) have recently been recognized as an important activator of the coagulation cascade, as well as an integral component of arterial and venous thrombi. This study was undertaken to determine whether aPL activate neutrophils to release NETs, thereby predisposing to the arterial and venous thrombosis inherent in the antiphospholipid syndrome (APS). METHODS: Neutrophils, sera, and plasma were prepared from patients with primary APS (n?=?52) or from healthy volunteers and characterized. No patient had concomitant systemic lupus erythematosus. RESULTS: Sera and plasma from patients with primary APS had elevated levels of both cell-free DNA and NETs, as compared to healthy volunteers. Freshly isolated neutrophils from patients with APS were predisposed to high levels of spontaneous NET release. Further, APS patient sera, as well as IgG purified from APS patients, stimulated NET release from control neutrophils. Human aPL monoclonal antibodies, especially those targeting ?2 GPI, also enhanced NET release. The induction of APS NETs was abrogated with inhibitors of reactive oxygen species formation and Toll-like receptor 4 signaling. Highlighting the potential clinical relevance of these findings, APS NETs promoted thrombin generation. CONCLUSION: Our findings indicate that NET release warrants further investigation as a novel therapeutic target in APS. Twit Text FOAVip Release of neutrophil extracellular traps by neutrophils stimulated with antiphospholipid antibodies: a newly identified mechanism of thrombosis in the antiphospholipid syndrome ????Arthritis Rheumatol http://www.kidney.de/pget.php?&tw=1&pmid=26097119 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26097119 #FOAvip English Wikipedia <ref>{{Cite pmid|26097119 }}</ref> Release of neutrophil extracellular traps by neutrophils stimulated with antiphospholipid antibodies: a newly identified mechanism of thrombosis in the antiphospholipid syndrome #MMPMID26097119 Yalavarthi S ; Gould TJ ; Rao AN ; Mazza LF ; Morris AE ; Núñez-Álvarez C ; Hernández-Ramírez D ; Bockenstedt PL ; Liaw PC ; Cabral AR ; Knight JS Arthritis Rheumatol 2015[Nov]; 67 (11 ): 2990-3003 PMID26097119 show ga OBJECTIVE: Antiphospholipid antibodies (aPL), especially those targeting ?2 -glycoprotein I (?2 GPI), are well known to activate endothelial cells, monocytes, and platelets, with prothrombotic implications. In contrast, the interaction of aPL with neutrophils has not been extensively studied. Neutrophil extracellular traps (NETs) have recently been recognized as an important activator of the coagulation cascade, as well as an integral component of arterial and venous thrombi. This study was undertaken to determine whether aPL activate neutrophils to release NETs, thereby predisposing to the arterial and venous thrombosis inherent in the antiphospholipid syndrome (APS). METHODS: Neutrophils, sera, and plasma were prepared from patients with primary APS (n?=?52) or from healthy volunteers and characterized. No patient had concomitant systemic lupus erythematosus. RESULTS: Sera and plasma from patients with primary APS had elevated levels of both cell-free DNA and NETs, as compared to healthy volunteers. Freshly isolated neutrophils from patients with APS were predisposed to high levels of spontaneous NET release. Further, APS patient sera, as well as IgG purified from APS patients, stimulated NET release from control neutrophils. Human aPL monoclonal antibodies, especially those targeting ?2 GPI, also enhanced NET release. The induction of APS NETs was abrogated with inhibitors of reactive oxygen species formation and Toll-like receptor 4 signaling. Highlighting the potential clinical relevance of these findings, APS NETs promoted thrombin generation. CONCLUSION: Our findings indicate that NET release warrants further investigation as a novel therapeutic target in APS. |*Extracellular Traps [MESH] |Antibodies, Antiphospholipid/*immunology [MESH] |Antiphospholipid Syndrome/*immunology/metabolism [MESH] |Humans [MESH] |Immunoglobulin G/immunology [MESH] |Neutrophils/*immunology/metabolism [MESH] |Reactive Oxygen Species/metabolism [MESH] |Signal Transduction/physiology [MESH] |Thrombosis/*immunology/metabolism [MESH]Release of neutrophil extracellular traps by neutrophils stimulated wi(epmc).pdf DeepDyve Pubget Overpricing