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10.1126/sciimmunol.aag3358 http://scihub22266oqcxt.onion/10.1126/sciimmunol.aag3358 28649674!5479641!28649674     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28649674&cmd=llinks): Failed to open stream: HTTP request failed! 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Synovial fibroblast-neutrophil interactions promote pathogenic adaptive immunity in rheumatoid arthritis |pdf=|usr=}}{{28649674}} gab.com Text Synovial fibroblast-neutrophil interactions promote pathogenic adaptive immunity in rheumatoid arthritis JO: Sci Immunol http://www.kidney.de/pget.php?&tw=1&pmid=28649674 #FOAvip Rheumatoid arthritis (RA) is characterized by synovial joint inflammation and by development of pathogenic humoral and cellular autoimmunity to citrullinated proteins. Neutrophil extracellular traps (NETs) are a source of citrullinated autoantigens and activate RA synovial fibroblasts (FLS), cells crucial in joint damage. We investigated the molecular mechanisms by which NETs promote proinflammatory phenotypes in FLS, and whether these interactions generate pathogenic anti-citrulline adaptive immune responses. NETs containing citrullinated peptides are internalized by FLS through a RAGE-TLR9 pathway promoting FLS inflammatory phenotype and their upregulation of MHC class II. Once internalized, arthritogenic NET-peptides are loaded into FLS MHC class II and presented to Ag-specific T cells. HLADRB1*0401 transgenic mice immunized with mouse FLS loaded with NETs develop antibodies specific to citrullinated forms of relevant RA autoantigens implicated in RA pathogenesis as well as cartilage damage. These results implicate FLS as mediators in RA pathogenesis, through the internalization and presentation of NET citrullinated peptides to the adaptive immune system leading to pathogenic autoimmunity and cartilage damage. Twit Text FOAVip Synovial fibroblast-neutrophil interactions promote pathogenic adaptive immunity in rheumatoid arthritis ????Sci Immunol http://www.kidney.de/pget.php?&tw=1&pmid=28649674 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28649674 #FOAvip English Wikipedia <ref>{{Cite pmid|28649674}}</ref> Synovial fibroblast-neutrophil interactions promote pathogenic adaptive immunity in rheumatoid arthritis #MMPMID28649674 Carmona-Rivera C; Carlucci PM; Moore E; Lingampalli N; Uchtenhagen H; James E; Liu Y; Bicker KL; Wahamaa H; Hoffmann V; Catrina AI; Thompson P; Buckner JH; Robinson WH; Fox DA; Kaplan MJ Sci Immunol 2017[Apr]; 2 (10): ä PMID28649674show ga Rheumatoid arthritis (RA) is characterized by synovial joint inflammation and by development of pathogenic humoral and cellular autoimmunity to citrullinated proteins. Neutrophil extracellular traps (NETs) are a source of citrullinated autoantigens and activate RA synovial fibroblasts (FLS), cells crucial in joint damage. We investigated the molecular mechanisms by which NETs promote proinflammatory phenotypes in FLS, and whether these interactions generate pathogenic anti-citrulline adaptive immune responses. NETs containing citrullinated peptides are internalized by FLS through a RAGE-TLR9 pathway promoting FLS inflammatory phenotype and their upregulation of MHC class II. Once internalized, arthritogenic NET-peptides are loaded into FLS MHC class II and presented to Ag-specific T cells. HLADRB1*0401 transgenic mice immunized with mouse FLS loaded with NETs develop antibodies specific to citrullinated forms of relevant RA autoantigens implicated in RA pathogenesis as well as cartilage damage. These results implicate FLS as mediators in RA pathogenesis, through the internalization and presentation of NET citrullinated peptides to the adaptive immune system leading to pathogenic autoimmunity and cartilage damage. äSynovial fibroblast-neutrophil interactions promote pathogenic adaptiv(epmc).pdf DeepDyve Pubget Overpricing