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10.1097/BOR.0000000000000087 http://scihub22266oqcxt.onion/10.1097/BOR.0000000000000087 25010440!4280994!25010440     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=25010440&cmd=llinks): Failed to open stream: HTTP request failed! 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Advances in understanding the role of type I interferons in systemic lupus erythematosus |pdf=|usr=}}{{25010440}} gab.com Text Advances in understanding the role of type I interferons in systemic lupus erythematosus JO: Curr Opin Rheumatol http://www.kidney.de/pget.php?&tw=1&pmid=25010440 #FOAvip PURPOSE OF REVIEW: Advances in understanding the genetic and molecular basis of innate immune system activation and function have supported the hypothesis that type I interferons (IFN-I), the essential mediators of antiviral host defense, are central contributors to the pathogenesis of systemic lupus erythematosus (SLE). This review addresses the recent data that support the rationale for therapeutic targeting of the IFN-I pathway in SLE. RECENT FINDINGS: New insights into the mechanisms of cell-intrinsic innate immune system activation, driven by endogenous virus-like nucleic acids and potentially modified by environmental stressors, provide a model for the induction of IFN-I that may precede the clinically apparent autoimmunity in patients with lupus. Further amplification of IFN-alpha production, induced by nucleic-acid-containing immune complexes that activate endosomal Toll-like receptors, augments and sustains immune system activation, autoimmunity and tissue damage. SUMMARY: As demonstrated in the murine studies of persistent virus infection accompanied by sustained production of IFN-I, blockade of the IFN-I pathway may reverse the immune dysregulation and tissue damage that are the essential features of the immunopathogenesis of SLE. Recent research progress has identified numerous therapeutic targets, and specific candidate therapeutics relevant to the IFN-I pathway are under investigation. Twit Text FOAVip Advances in understanding the role of type I interferons in systemic lupus erythematosus ????Curr Opin Rheumatol http://www.kidney.de/pget.php?&tw=1&pmid=25010440 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25010440 #FOAvip English Wikipedia <ref>{{Cite pmid|25010440}}</ref> Advances in understanding the role of type I interferons in systemic lupus erythematosus #MMPMID25010440 Crow MK Curr Opin Rheumatol 2014[Sep]; 26 (5): 467-74 PMID25010440show ga PURPOSE OF REVIEW: Advances in understanding the genetic and molecular basis of innate immune system activation and function have supported the hypothesis that type I interferons (IFN-I), the essential mediators of antiviral host defense, are central contributors to the pathogenesis of systemic lupus erythematosus (SLE). This review addresses the recent data that support the rationale for therapeutic targeting of the IFN-I pathway in SLE. RECENT FINDINGS: New insights into the mechanisms of cell-intrinsic innate immune system activation, driven by endogenous virus-like nucleic acids and potentially modified by environmental stressors, provide a model for the induction of IFN-I that may precede the clinically apparent autoimmunity in patients with lupus. Further amplification of IFN-alpha production, induced by nucleic-acid-containing immune complexes that activate endosomal Toll-like receptors, augments and sustains immune system activation, autoimmunity and tissue damage. SUMMARY: As demonstrated in the murine studies of persistent virus infection accompanied by sustained production of IFN-I, blockade of the IFN-I pathway may reverse the immune dysregulation and tissue damage that are the essential features of the immunopathogenesis of SLE. Recent research progress has identified numerous therapeutic targets, and specific candidate therapeutics relevant to the IFN-I pathway are under investigation. |Animals[MESH] |Autoimmunity/genetics[MESH] |Genetic Association Studies[MESH] |Humans[MESH] |Immunity, Innate[MESH] |Interferon Type I/antagonists & inhibitors/genetics/*metabolism[MESH] |Lupus Erythematosus, Systemic/etiology/*immunology/therapy[MESH] |Mice[MESH] |Models, Immunological[MESH] |Neutrophils/immunology[MESH] |Receptor, Interferon alpha-beta/antagonists & inhibitors[MESH]Advances in understanding the role of type I interferons in systemic l(epmc).pdf DeepDyve Pubget Overpricing