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10.3389/fimmu.2019.01028 http://scihub22266oqcxt.onion/10.3389/fimmu.2019.01028 31139185!6519310!31139185     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=31139185&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 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\31139185.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Front+Immunol 2019 ; 10 (ä): 1028 Nephropedia Template TP {{tp|p=31139185|t=2019. Sources of Pathogenic Nucleic Acids in Systemic Lupus Erythematosus |pdf=|usr=}}{{31139185}} gab.com Text Sources of Pathogenic Nucleic Acids in Systemic Lupus Erythematosus JO: Front Immunol http://www.kidney.de/pget.php?&tw=1&pmid=31139185 #FOAvip A hallmark of systemic lupus erythematosus (SLE), and several related autoimmune diseases, is the presence of autoantibodies against nucleic acids and nucleic acid-binding proteins, as well as elevated type I interferons (IFNs), which appear to be instrumental in disease pathogenesis. Here we discuss the sources and proposed mechanisms by which a range of cellular RNA and DNA species can become pathogenic and trigger the nucleic acid sensors that drive type I interferon production. Potentially SLE-promoting DNA may originate from pieces of chromatin, from mitochondria, or from reverse-transcribed cellular RNA, while pathogenic RNA may arise from mis-localized, mis-processed, ancient retroviral, or transposable element-derived transcripts. These nucleic acids may leak out from dying cells to be internalized and reacted to by immune cells or they may be generated and remain to be sensed intracellularly in immune or non-immune cells. The presence of aberrant DNA or RNA is normally counteracted by effective counter-mechanisms, the loss of which result in a serious type I IFN-driven disease called Aicardi-Goutieres Syndrome. However, in SLE it remains unclear which mechanisms are most critical in precipitating disease: aberrant RNA or DNA, overly sensitive sensor mechanisms, or faulty counter-acting defenses. We propose that the clinical heterogeneity of SLE may be reflected, in part, by heterogeneity in which pathogenic nucleic acid molecules are present and which sensors and pathways they trigger in individual patients. Elucidation of these events may result in the recognition of distinct "endotypes" of SLE, each with its distinct therapeutic choices. Twit Text FOAVip Sources of Pathogenic Nucleic Acids in Systemic Lupus Erythematosus ????Front Immunol http://www.kidney.de/pget.php?&tw=1&pmid=31139185 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=31139185 #FOAvip English Wikipedia <ref>{{Cite pmid|31139185}}</ref> Sources of Pathogenic Nucleic Acids in Systemic Lupus Erythematosus #MMPMID31139185 Mustelin T; Lood C; Giltiay NV Front Immunol 2019[]; 10 (ä): 1028 PMID31139185show ga A hallmark of systemic lupus erythematosus (SLE), and several related autoimmune diseases, is the presence of autoantibodies against nucleic acids and nucleic acid-binding proteins, as well as elevated type I interferons (IFNs), which appear to be instrumental in disease pathogenesis. Here we discuss the sources and proposed mechanisms by which a range of cellular RNA and DNA species can become pathogenic and trigger the nucleic acid sensors that drive type I interferon production. Potentially SLE-promoting DNA may originate from pieces of chromatin, from mitochondria, or from reverse-transcribed cellular RNA, while pathogenic RNA may arise from mis-localized, mis-processed, ancient retroviral, or transposable element-derived transcripts. These nucleic acids may leak out from dying cells to be internalized and reacted to by immune cells or they may be generated and remain to be sensed intracellularly in immune or non-immune cells. The presence of aberrant DNA or RNA is normally counteracted by effective counter-mechanisms, the loss of which result in a serious type I IFN-driven disease called Aicardi-Goutieres Syndrome. However, in SLE it remains unclear which mechanisms are most critical in precipitating disease: aberrant RNA or DNA, overly sensitive sensor mechanisms, or faulty counter-acting defenses. We propose that the clinical heterogeneity of SLE may be reflected, in part, by heterogeneity in which pathogenic nucleic acid molecules are present and which sensors and pathways they trigger in individual patients. Elucidation of these events may result in the recognition of distinct "endotypes" of SLE, each with its distinct therapeutic choices. |*Lupus Erythematosus, Systemic/etiology/immunology/pathology/therapy[MESH] |Animals[MESH] |Autoimmune Diseases of the Nervous System/complications/immunology/pathology[MESH] |DNA/*immunology[MESH] |Humans[MESH] |Interferon Type I/immunology[MESH] |Nervous System Malformations/complications/immunology/pathology[MESH]Sources of Pathogenic Nucleic Acids in Systemic Lupus Erythematosus (epmc).pdf DeepDyve Pubget Overpricing