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10.3389/fimmu.2015.00291 http://scihub22266oqcxt.onion/10.3389/fimmu.2015.00291 C4456949!4456949 !26097482     free     free     free Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\26097482 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Front+Immunol 2015 ; 6 (ä): 291 Nephropedia Template TP {{tp|p=26097482 |t=2015. Animal Models of Interferon Signature Positive Lupus |pdf=|usr=}}{{26097482 }} gab.com Text Animal Models of Interferon Signature Positive Lupus JO: Front Immunol http://www.kidney.de/pget.php?&tw=1&pmid=26097482 #FOAvip Human lupus is strongly associated with a gene expression signature characterized by over-expression of Type I interferon-regulated genes. A strong interferon signature generally is not seen in the standard mouse models of lupus, despite considerable evidence for the involvement of toll-like receptor-driven interferon production. In contrast, pristane-induced lupus exhibits a prominent TLR7-dependent interferon signature. Importantly, genetic disorders with dysregulated interferon production in both human beings and mice cause severe autoinflammatory diseases but not the typical manifestations of lupus, suggesting that interferon over-production is insufficient to cause systemic lupus erythematosus itself. Single-gene models in mice suggest that lupus-like disease may result from abnormalities in B-cell activation and the clearance of dead cells. Pristane may mimic human systemic lupus erythematosus by causing synergistic abnormalities in interferon production along with defective clearance of apoptotic cells and over-active B-cell signaling. Twit Text FOAVip Animal Models of Interferon Signature Positive Lupus ????Front Immunol http://www.kidney.de/pget.php?&tw=1&pmid=26097482 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26097482 #FOAvip English Wikipedia <ref>{{Cite pmid|26097482 }}</ref> Animal Models of Interferon Signature Positive Lupus #MMPMID26097482 Zhuang H ; Szeto C ; Han S ; Yang L ; Reeves WH Front Immunol 2015[]; 6 (ä): 291 PMID26097482 show ga Human lupus is strongly associated with a gene expression signature characterized by over-expression of Type I interferon-regulated genes. A strong interferon signature generally is not seen in the standard mouse models of lupus, despite considerable evidence for the involvement of toll-like receptor-driven interferon production. In contrast, pristane-induced lupus exhibits a prominent TLR7-dependent interferon signature. Importantly, genetic disorders with dysregulated interferon production in both human beings and mice cause severe autoinflammatory diseases but not the typical manifestations of lupus, suggesting that interferon over-production is insufficient to cause systemic lupus erythematosus itself. Single-gene models in mice suggest that lupus-like disease may result from abnormalities in B-cell activation and the clearance of dead cells. Pristane may mimic human systemic lupus erythematosus by causing synergistic abnormalities in interferon production along with defective clearance of apoptotic cells and over-active B-cell signaling. äAnimal Models of Interferon Signature Positive Lupus (epmc).pdf DeepDyve Pubget Overpricing