Use my Search Websuite to scan PubMed, PMCentral, Journal Hosts and Journal Archives, FullText. Kick-your-searchterm to multiple Engines kick-your-query now !>

A dictionary by aggregated review articles of nephrology, medicine and the life sciences Your one-stop-run pathway from word to the immediate pdf of peer-reviewed on-topic knowledge.

10.1038/mi.2015.34 http://scihub22266oqcxt.onion/10.1038/mi.2015.34 C4626445!4626445!25921340     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       Mucosal+Immunol 2016 ; 9 (1): 38-55 Nephropedia Template TP {{tp|p=25921340|t=2016. Macrophages are critical to the maintenance of IL-13-dependent lung inflammation and fibrosis |pdf=|usr=}}{{25921340}} gab.com Text Macrophages are critical to the maintenance of IL-13-dependent lung inflammation and fibrosis JO: Mucosal Immunol http://www.kidney.de/pget.php?&tw=1&pmid=25921340 #FOAvip The roles of macrophages in type 2-driven inflammation and fibrosis remain unclear. Here, using CD11b-Diphtheria Toxin Receptor (DTR) transgenic mice and three models of IL-13-dependent inflammation, fibrosis, and immunity, we show that CD11b+ F4/80+ Ly6C+ macrophages are required for the maintenance of type-2 immunity within affected tissues but not secondary lymphoid organs. Direct depletion of macrophages during the maintenance or resolution phases of secondary S. mansoni egg-induced granuloma formation caused a profound decrease in inflammation, fibrosis, and type-2 gene expression. Additional studies with CD11c-DTR and CD11b/CD11c-DTR double transgenic mice suggested that macrophages but not dendritic cells were critical. Mechanistically, macrophage depletion impaired effector CD4+ Th2 cell homing and activation within the inflamed lung. Depletion of CD11b+ F4/80+ Ly6C+ macrophages similarly reduced house dust mite-induced allergic lung inflammation and suppressed IL-13-dependent immunity to the nematode parasite Nippostrongylus brasiliensis. Consequently, therapeutic strategies targeting macrophages offer a novel approach to ameliorate established type-2 inflammatory diseases. Twit Text FOAVip Macrophages are critical to the maintenance of IL-13-dependent lung inflammation and fibrosis ????Mucosal Immunol http://www.kidney.de/pget.php?&tw=1&pmid=25921340 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25921340 #FOAvip English Wikipedia <ref>{{Cite pmid|25921340}}</ref> Macrophages are critical to the maintenance of IL-13-dependent lung inflammation and fibrosis #MMPMID25921340 Borthwick LA; Barron L; Hart KM; Vannella KM; Thompson RW; Oland S; Cheever A; Sciurba J; Ramalingam TR; Fisher AJ; Wynn TA Mucosal Immunol 2016[Jan]; 9 (1): 38-55 PMID25921340show ga The roles of macrophages in type 2-driven inflammation and fibrosis remain unclear. Here, using CD11b-Diphtheria Toxin Receptor (DTR) transgenic mice and three models of IL-13-dependent inflammation, fibrosis, and immunity, we show that CD11b+ F4/80+ Ly6C+ macrophages are required for the maintenance of type-2 immunity within affected tissues but not secondary lymphoid organs. Direct depletion of macrophages during the maintenance or resolution phases of secondary S. mansoni egg-induced granuloma formation caused a profound decrease in inflammation, fibrosis, and type-2 gene expression. Additional studies with CD11c-DTR and CD11b/CD11c-DTR double transgenic mice suggested that macrophages but not dendritic cells were critical. Mechanistically, macrophage depletion impaired effector CD4+ Th2 cell homing and activation within the inflamed lung. Depletion of CD11b+ F4/80+ Ly6C+ macrophages similarly reduced house dust mite-induced allergic lung inflammation and suppressed IL-13-dependent immunity to the nematode parasite Nippostrongylus brasiliensis. Consequently, therapeutic strategies targeting macrophages offer a novel approach to ameliorate established type-2 inflammatory diseases. äMacrophages are critical to the maintenance of IL-13-dependent lung in(epmc).pdf DeepDyve Pubget Overpricing