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10.1016/j.immuni.2015.06.002 http://scihub22266oqcxt.onion/10.1016/j.immuni.2015.06.002 C4500125!4500125!26084027     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26084027&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\26084027.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Immunity 2015 ; 42 (6): 1171-84 Nephropedia Template TP {{tp|p=26084027|t=2015. Amyloid-DNA composites of bacterial biofilms stimulate autoimmunity |pdf=|usr=}}{{26084027}} gab.com Text Amyloid-DNA composites of bacterial biofilms stimulate autoimmunity JO: Immunity http://www.kidney.de/pget.php?&tw=1&pmid=26084027 #FOAvip Research on the human microbiome has established that commensal and pathogenic bacteria can influence obesity, cancer, and autoimmunity through mechanisms mostly unknown. We found that a component of bacterial biofilms, the amyloid protein curli, irreversibly formed fibers with bacterial DNA during biofilm formation. This interaction accelerated amyloid polymerization and created potent immunogenic complexes that activated immune cells, including dendritic cells, to produce cytokines such as Type I interferons, which are pathogenic in systemic lupus erythematosus (SLE). When given systemically, curli-DNA composites triggered immune activation and production of autoantibodies in lupus-prone and wild-type mice. We also found that the infection of lupus-prone mice with curli-producing bacteria triggered higher autoantibody titers compared to curli-deficient bacteria. These data provide a mechanism by which the microbiome and biofilm-producing enteric infections may contribute to the progression of SLE and point to a potential molecular target for treatment of autoimmunity. Twit Text FOAVip Amyloid-DNA composites of bacterial biofilms stimulate autoimmunity ????Immunity http://www.kidney.de/pget.php?&tw=1&pmid=26084027 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26084027 #FOAvip English Wikipedia <ref>{{Cite pmid|26084027}}</ref> Amyloid-DNA composites of bacterial biofilms stimulate autoimmunity #MMPMID26084027 Gallo PM; Rapsinski GJ; Wilson RP; Oppong GO; Sriram U; Goulian M; Buttaro B; Caricchio R; Gallucci S; Tükel Ç Immunity 2015[Jun]; 42 (6): 1171-84 PMID26084027show ga Research on the human microbiome has established that commensal and pathogenic bacteria can influence obesity, cancer, and autoimmunity through mechanisms mostly unknown. We found that a component of bacterial biofilms, the amyloid protein curli, irreversibly formed fibers with bacterial DNA during biofilm formation. This interaction accelerated amyloid polymerization and created potent immunogenic complexes that activated immune cells, including dendritic cells, to produce cytokines such as Type I interferons, which are pathogenic in systemic lupus erythematosus (SLE). When given systemically, curli-DNA composites triggered immune activation and production of autoantibodies in lupus-prone and wild-type mice. We also found that the infection of lupus-prone mice with curli-producing bacteria triggered higher autoantibody titers compared to curli-deficient bacteria. These data provide a mechanism by which the microbiome and biofilm-producing enteric infections may contribute to the progression of SLE and point to a potential molecular target for treatment of autoimmunity. äAmyloid-DNA composites of bacterial biofilms stimulate autoimmunity (epmc).pdf DeepDyve Pubget Overpricing