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10.4049/jimmunol.1002795 http://scihub22266oqcxt.onion/10.4049/jimmunol.1002795 24907379!4083591!24907379     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=24907379&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 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\24907379.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       J+Immunol 2014 ; 192 (12): 5459-68 Nephropedia Template TP {{tp|p=24907379|t=2014. Type I interferon in the pathogenesis of lupus |pdf=|usr=}}{{24907379}} gab.com Text Type I interferon in the pathogenesis of lupus JO: J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=24907379 #FOAvip Investigations of patients with systemic lupus erythematosus have applied insights from studies of the innate immune response to define IFN-I, with IFN-alpha as the dominant mediator, as central to the pathogenesis of this prototype systemic autoimmune disease. Genetic association data identify regulators of nucleic acid degradation and components of TLR-independent, endosomal TLR-dependent, and IFN-I-signaling pathways as contributors to lupus disease susceptibility. Together with a gene expression signature characterized by IFN-I-induced gene transcripts in lupus blood and tissue, those data support the conclusion that many of the immunologic and pathologic features of this disease are a consequence of a persistent self-directed immune reaction driven by IFN-I and mimicking a sustained antivirus response. This expanding knowledge of the role of IFN-I and the innate immune response suggests candidate therapeutic targets that are being tested in lupus patients. Twit Text FOAVip Type I interferon in the pathogenesis of lupus ????J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=24907379 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24907379 #FOAvip English Wikipedia <ref>{{Cite pmid|24907379}}</ref> Type I interferon in the pathogenesis of lupus #MMPMID24907379 Crow MK J Immunol 2014[Jun]; 192 (12): 5459-68 PMID24907379show ga Investigations of patients with systemic lupus erythematosus have applied insights from studies of the innate immune response to define IFN-I, with IFN-alpha as the dominant mediator, as central to the pathogenesis of this prototype systemic autoimmune disease. Genetic association data identify regulators of nucleic acid degradation and components of TLR-independent, endosomal TLR-dependent, and IFN-I-signaling pathways as contributors to lupus disease susceptibility. Together with a gene expression signature characterized by IFN-I-induced gene transcripts in lupus blood and tissue, those data support the conclusion that many of the immunologic and pathologic features of this disease are a consequence of a persistent self-directed immune reaction driven by IFN-I and mimicking a sustained antivirus response. This expanding knowledge of the role of IFN-I and the innate immune response suggests candidate therapeutic targets that are being tested in lupus patients. |*Immunity, Innate[MESH] |Animals[MESH] |Gene Expression Regulation/*immunology[MESH] |Humans[MESH] |Interferon Type I/*immunology[MESH] |Lupus Erythematosus, Systemic/blood/*immunology[MESH]Type I interferon in the pathogenesis of lupus (epmc).pdf DeepDyve Pubget Overpricing