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10.1172/JCI78086 http://scihub22266oqcxt.onion/10.1172/JCI78086 C4497748!4497748 !26030227     free     free     free Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\26030227 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       J+Clin+Invest 2015 ; 125 (6 ): 2234-41 Nephropedia Template TP {{tp|p=26030227 |t=2015. Genetic basis of autoimmunity |pdf=|usr=}}{{26030227 }} gab.com Text Genetic basis of autoimmunity JO: J Clin Invest http://www.kidney.de/pget.php?&tw=1&pmid=26030227 #FOAvip Autoimmune diseases affect up to approximately 10% of the population. While rare Mendelian autoimmunity syndromes can result from monogenic mutations disrupting essential mechanisms of central and peripheral tolerance, more common human autoimmune diseases are complex disorders that arise from the interaction between polygenic risk factors and environmental factors. Although the risk attributable to most individual nucleotide variants is modest, genome-wide association studies (GWAS) have the potential to provide an unbiased view of biological pathways that drive human autoimmune diseases. Interpretation of GWAS requires integration of multiple genomic datasets including dense genotyping, cis-regulatory maps of primary immune cells, and genotyped studies of gene expression in relevant cell types and cellular conditions. Improved understanding of the genetic basis of autoimmunity may lead to a more sophisticated understanding of underlying cellular phenotypes and, eventually, novel diagnostics and targeted therapies. Twit Text FOAVip Genetic basis of autoimmunity ????J Clin Invest http://www.kidney.de/pget.php?&tw=1&pmid=26030227 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26030227 #FOAvip English Wikipedia <ref>{{Cite pmid|26030227 }}</ref> Genetic basis of autoimmunity #MMPMID26030227 Marson A ; Housley WJ ; Hafler DA J Clin Invest 2015[Jun]; 125 (6 ): 2234-41 PMID26030227 show ga Autoimmune diseases affect up to approximately 10% of the population. While rare Mendelian autoimmunity syndromes can result from monogenic mutations disrupting essential mechanisms of central and peripheral tolerance, more common human autoimmune diseases are complex disorders that arise from the interaction between polygenic risk factors and environmental factors. Although the risk attributable to most individual nucleotide variants is modest, genome-wide association studies (GWAS) have the potential to provide an unbiased view of biological pathways that drive human autoimmune diseases. Interpretation of GWAS requires integration of multiple genomic datasets including dense genotyping, cis-regulatory maps of primary immune cells, and genotyped studies of gene expression in relevant cell types and cellular conditions. Improved understanding of the genetic basis of autoimmunity may lead to a more sophisticated understanding of underlying cellular phenotypes and, eventually, novel diagnostics and targeted therapies. |*Databases, Genetic [MESH] |*Gene-Environment Interaction [MESH] |Animals [MESH] |Autoimmune Diseases/*genetics/*immunology [MESH] |Autoimmunity/*genetics [MESH] |Gene Expression Regulation/*immunology [MESH] |Genome-Wide Association Study [MESH]Genetic basis of autoimmunity (epmc).pdf DeepDyve Pubget Overpricing