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10.1189/jlb.1006652 http://scihub22266oqcxt.onion/10.1189/jlb.1006652 C4492281!4492281!17576821     free     free     free Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 247.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 247.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Leukoc+Biol 2007 ; 82 (3): 721-8 Nephropedia Template TP {{tp|p=17576821|t=2007. Fas (CD95) Induces Macrophage Pro-Inflammatory Chemokine Production via a MyD88-dependent, Caspase-independent Pathway |pdf=|usr=}}{{17576821}} gab.com Text Fas (CD95) Induces Macrophage Pro-Inflammatory Chemokine Production via a MyD88-dependent, Caspase-independent Pathway JO: J Leukoc Biol http://www.kidney.de/pget.php?&tw=1&pmid=17576821 #FOAvip Activation of the prototypical death receptor, Fas (CD95), can induce both caspase-dependent cell death and production of pro-inflammatory chemokines, leading to neutrophil recruitment and end-organ injury. The precise mechanism(s), by which Fas upregulates chemokine production and release, is currently unclear. We hypothesized that Fas-induced chemokine release by macrophages is dependent on the MyD88 adapter molecule and independent of caspase activity. To test this hypothesis, we measured chemokine response to Fas activation both in RAW 264.7 cells with RNAi-attenuated MyD88 expression and in MyD88-deficient primary macrophages. We found that Fas-induced chemokine release was abrogated in the absence of MyD88. In vivo, MyD88?/? mice had impaired CXCL1/KC release and polymorphonuclear cell recruitment in response to intratracheal treatment with the Fas-activating monoclonal antibody, Jo-2. Furthermore, Fas-induced chemokine release was not dependent on either IL-1 receptor signaling or on caspase activity. We conclude that MyD88 plays an integral role in Fas-induced macrophage-mediated inflammation. Twit Text FOAVip Fas (CD95) Induces Macrophage Pro-Inflammatory Chemokine Production via a MyD88-dependent, Caspase-independent Pathway ????J Leukoc Biol http://www.kidney.de/pget.php?&tw=1&pmid=17576821 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=17576821 #FOAvip English Wikipedia <ref>{{Cite pmid|17576821}}</ref> Fas (CD95) Induces Macrophage Pro-Inflammatory Chemokine Production via a MyD88-dependent, Caspase-independent Pathway #MMPMID17576821 Altemeier WA; Zhu X; Berrington WR; Harlan JM; Liles WC J Leukoc Biol 2007[Sep]; 82 (3): 721-8 PMID17576821show ga Activation of the prototypical death receptor, Fas (CD95), can induce both caspase-dependent cell death and production of pro-inflammatory chemokines, leading to neutrophil recruitment and end-organ injury. The precise mechanism(s), by which Fas upregulates chemokine production and release, is currently unclear. We hypothesized that Fas-induced chemokine release by macrophages is dependent on the MyD88 adapter molecule and independent of caspase activity. To test this hypothesis, we measured chemokine response to Fas activation both in RAW 264.7 cells with RNAi-attenuated MyD88 expression and in MyD88-deficient primary macrophages. We found that Fas-induced chemokine release was abrogated in the absence of MyD88. In vivo, MyD88?/? mice had impaired CXCL1/KC release and polymorphonuclear cell recruitment in response to intratracheal treatment with the Fas-activating monoclonal antibody, Jo-2. Furthermore, Fas-induced chemokine release was not dependent on either IL-1 receptor signaling or on caspase activity. We conclude that MyD88 plays an integral role in Fas-induced macrophage-mediated inflammation. äFas (CD95) Induces Macrophage Pro-Inflammatory Chemokine Production vi(epmc).pdf DeepDyve Pubget Overpricing