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10.1038/nm1303 http://scihub22266oqcxt.onion/10.1038/nm1303 C6322907!6322907!16208318     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Nat+Med 2005 ; 11 (11): 1180-7 Nephropedia Template TP {{tp|p=16208318|t=2005. CCL5-CCR5 interaction provides antiapoptotic signals for macrophage survival during viral infection |pdf=|usr=}}{{16208318}} gab.com Text CCL5-CCR5 interaction provides antiapoptotic signals for macrophage survival during viral infection JO: Nat Med http://www.kidney.de/pget.php?&tw=1&pmid=16208318 #FOAvip Host defense against viruses probably depends on targeted death of infected host cells and then clearance of cellular corpses by macrophages. For this process to be effective, the macrophage must presumably avoid its own virus-induced death. Here we identify one such mechanism. We show that mice lacking the chemokine Ccl5 are immune compromised to the point of delayed viral clearance, excessive airway inflammation and respiratory death after mouse parainfluenza or human influenza virus infection. Virus-inducible levels of Ccl5 are required to prevent apoptosis of virus-infected mouse macrophages in vivo and mouse and human macrophages ex vivo. The protective effect of Ccl5 requires activation of the Ccr5 chemokine receptor and consequent bilateral activation of G?i-PI3K-AKT and G?i-MEK-ERK signaling pathways. The antiapoptotic action of chemokine signaling may therefore allow scavengers to finally stop the host cell-to-cell infectious process. Twit Text FOAVip CCL5-CCR5 interaction provides antiapoptotic signals for macrophage survival during viral infection ????Nat Med http://www.kidney.de/pget.php?&tw=1&pmid=16208318 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=16208318 #FOAvip English Wikipedia <ref>{{Cite pmid|16208318}}</ref> CCL5-CCR5 interaction provides antiapoptotic signals for macrophage survival during viral infection #MMPMID16208318 Tyner JW; Uchida O; Kajiwara N; Kim EY; Patel AC; O?Sullivan MP; Walter MJ; Schwendener RA; Cook DN; Danoff TM; Holtzman MJ Nat Med 2005[Nov]; 11 (11): 1180-7 PMID16208318show ga Host defense against viruses probably depends on targeted death of infected host cells and then clearance of cellular corpses by macrophages. For this process to be effective, the macrophage must presumably avoid its own virus-induced death. Here we identify one such mechanism. We show that mice lacking the chemokine Ccl5 are immune compromised to the point of delayed viral clearance, excessive airway inflammation and respiratory death after mouse parainfluenza or human influenza virus infection. Virus-inducible levels of Ccl5 are required to prevent apoptosis of virus-infected mouse macrophages in vivo and mouse and human macrophages ex vivo. The protective effect of Ccl5 requires activation of the Ccr5 chemokine receptor and consequent bilateral activation of G?i-PI3K-AKT and G?i-MEK-ERK signaling pathways. The antiapoptotic action of chemokine signaling may therefore allow scavengers to finally stop the host cell-to-cell infectious process. äCCL5-CCR5 interaction provides antiapoptotic signals for macrophage su(epmc).pdf DeepDyve Pubget Overpricing