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10.1177/0961203310371161 http://scihub22266oqcxt.onion/10.1177/0961203310371161 20693194!3658279!20693194     free     free     free Deprecated: Implicit conversion from float 211.6 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\20693194.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Lupus 2010 ; 19 (9): 1012-9 Nephropedia Template TP {{tp|p=20693194|t=2010. The interferon-alpha signature of systemic lupus erythematosus |pdf=|usr=}}{{20693194}} gab.com Text The interferon-alpha signature of systemic lupus erythematosus JO: Lupus http://www.kidney.de/pget.php?&tw=1&pmid=20693194 #FOAvip Systemic lupus erythematosus (SLE) is a prototypic multisystem autoimmune disorder where interplay of environmental and genetic risk factors leads to progressive loss of tolerance to nuclear antigens over time, finally culminating in clinical disease. The heterogeneity of clinical manifestations and the disease's unpredictable course characterized by flares and remissions are very likely a reflection of heterogeneity at the origin of disease, with a final common pathway leading to loss of tolerance to nuclear antigens. Impaired clearance of immune complexes and apoptotic material and production of autoantibodies have long been recognized as major pathogenic events in this disease. Over the past decade the type I interferon cytokine family has been postulated to play a central role in SLE pathogenesis, by promoting feedback loops progressively disrupting peripheral immune tolerance and driving disease activity. The identification of key molecules involved in the pathogenesis of SLE will not only improve our understanding of this complex disease, but also help to identify novel targets for biological intervention. Twit Text FOAVip The interferon-alpha signature of systemic lupus erythematosus ????Lupus http://www.kidney.de/pget.php?&tw=1&pmid=20693194 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=20693194 #FOAvip English Wikipedia <ref>{{Cite pmid|20693194}}</ref> The interferon-alpha signature of systemic lupus erythematosus #MMPMID20693194 Obermoser G; Pascual V Lupus 2010[Aug]; 19 (9): 1012-9 PMID20693194show ga Systemic lupus erythematosus (SLE) is a prototypic multisystem autoimmune disorder where interplay of environmental and genetic risk factors leads to progressive loss of tolerance to nuclear antigens over time, finally culminating in clinical disease. The heterogeneity of clinical manifestations and the disease's unpredictable course characterized by flares and remissions are very likely a reflection of heterogeneity at the origin of disease, with a final common pathway leading to loss of tolerance to nuclear antigens. Impaired clearance of immune complexes and apoptotic material and production of autoantibodies have long been recognized as major pathogenic events in this disease. Over the past decade the type I interferon cytokine family has been postulated to play a central role in SLE pathogenesis, by promoting feedback loops progressively disrupting peripheral immune tolerance and driving disease activity. The identification of key molecules involved in the pathogenesis of SLE will not only improve our understanding of this complex disease, but also help to identify novel targets for biological intervention. |Animals[MESH] |Antigens, Nuclear/immunology[MESH] |Apoptosis/immunology[MESH] |Autoantibodies/immunology[MESH] |Humans[MESH] |Immune Tolerance[MESH] |Interferon Type I/*immunology[MESH] |Interferon-alpha/*immunology[MESH]The interferon-alpha signature of systemic lupus erythematosus (epmc).pdf DeepDyve Pubget Overpricing