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10.1146/annurev-immunol-031210-101405 http://scihub22266oqcxt.onion/10.1146/annurev-immunol-031210-101405 C4067317!4067317!21219188     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 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Annu+Rev+Immunol 2011 ; 29 (ä): 707-35 Nephropedia Template TP {{tp|p=21219188|t=2011. The Inflammasome NLRs in Immunity, Inflammation, and Associated Diseases |pdf=|usr=}}{{21219188}} gab.com Text The Inflammasome NLRs in Immunity, Inflammation, and Associated Diseases JO: Annu Rev Immunol http://www.kidney.de/pget.php?&tw=1&pmid=21219188 #FOAvip Inflammasome activation leads to caspase-1 activation, which causes the maturation cleavage of pro-IL-1? and pro-IL-18. A subgroup of the NLR (nucleotide-binding domain, leucine-rich repeat containing) proteins are key mediators of the inflammasome. Studies of gene-deficient mice and cells have implicated NLR inflammasomes in a host of responses to a wide range of microbial pathogens, inflammatory diseases, cancer, and metabolic and autoimmune disorders. Determining exactly how the inflammasome is activated in these diseases and disease models remains a challenge. This review presents and integrates recent progress in the field. Twit Text FOAVip The Inflammasome NLRs in Immunity, Inflammation, and Associated Diseases ????Annu Rev Immunol http://www.kidney.de/pget.php?&tw=1&pmid=21219188 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=21219188 #FOAvip English Wikipedia <ref>{{Cite pmid|21219188}}</ref> The Inflammasome NLRs in Immunity, Inflammation, and Associated Diseases #MMPMID21219188 Davis BK; Wen H; Ting JPY Annu Rev Immunol 2011[]; 29 (ä): 707-35 PMID21219188show ga Inflammasome activation leads to caspase-1 activation, which causes the maturation cleavage of pro-IL-1? and pro-IL-18. A subgroup of the NLR (nucleotide-binding domain, leucine-rich repeat containing) proteins are key mediators of the inflammasome. Studies of gene-deficient mice and cells have implicated NLR inflammasomes in a host of responses to a wide range of microbial pathogens, inflammatory diseases, cancer, and metabolic and autoimmune disorders. Determining exactly how the inflammasome is activated in these diseases and disease models remains a challenge. This review presents and integrates recent progress in the field. äThe Inflammasome NLRs in Immunity, Inflammation, and Associated Diseas(epmc).pdf DeepDyve Pubget Overpricing