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10.4049/jimmunol.1203362 http://scihub22266oqcxt.onion/10.4049/jimmunol.1203362 C3725733!3725733!23630359     free     free     free Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Immunol 2013 ; 190 (11): 5731-8 Nephropedia Template TP {{tp|p=23630359|t=2013. TGF?1 limits the onset of innate lung inflammation by promoting mast cell-derived IL-61 |pdf=|usr=}}{{23630359}} gab.com Text TGF 1 limits the onset of innate lung inflammation by promoting mast cell-derived IL-61 JO: J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=23630359 #FOAvip TGF?1 is an important suppressive mediator of inflammation but can also drive fibrosis and remodeling in the lung. In response to intratracheal LPS, neutrophils migrate into the lung and TGF?1 has been suggested to protect against the ensuing injury. However, the mechanisms for this protective role remain unknown. Using a model of acute lung injury (ALI), we demonstrate that TGF?1 decreases neutrophil numbers during the onset of injury. This was due to increased apoptosis, rather than less migration. We demonstrate that TGF?1 does not directly regulate neutrophil apoptosis, but instead functions through IL-6 to promote neutrophil clearance. Recombinant IL-6 is sufficient to promote neutrophil apoptosis and reduce neutrophilia in brochoalveolar lavage fluid while IL-6 is rapidly elevated following LPS-induced injury. Mast cells are a critical source of the IL-6, as mast cell deficient mice exhibit increased neutrophil numbers that is reduced by reconstitution with WT, but not IL-6?/?, mast cells. While IL-6 diminishes neutrophilia in mast cell-deficient mice, TGF?1 is ineffective, suggesting that these effects were mast cell dependent. Taken together, our findings establish a novel pathway through which TGF?1, likely derived from resident Tregs, controls the severity and magnitude of early innate inflammation by promoting IL-6 from mast cells. Twit Text FOAVip TGF 1 limits the onset of innate lung inflammation by promoting mast cell-derived IL-61 ????J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=23630359 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=23630359 #FOAvip English Wikipedia <ref>{{Cite pmid|23630359}}</ref> TGF?1 limits the onset of innate lung inflammation by promoting mast cell-derived IL-61 #MMPMID23630359 Ganeshan K; Johnston LK; Bryce PJ J Immunol 2013[Jun]; 190 (11): 5731-8 PMID23630359show ga TGF?1 is an important suppressive mediator of inflammation but can also drive fibrosis and remodeling in the lung. In response to intratracheal LPS, neutrophils migrate into the lung and TGF?1 has been suggested to protect against the ensuing injury. However, the mechanisms for this protective role remain unknown. Using a model of acute lung injury (ALI), we demonstrate that TGF?1 decreases neutrophil numbers during the onset of injury. This was due to increased apoptosis, rather than less migration. We demonstrate that TGF?1 does not directly regulate neutrophil apoptosis, but instead functions through IL-6 to promote neutrophil clearance. Recombinant IL-6 is sufficient to promote neutrophil apoptosis and reduce neutrophilia in brochoalveolar lavage fluid while IL-6 is rapidly elevated following LPS-induced injury. Mast cells are a critical source of the IL-6, as mast cell deficient mice exhibit increased neutrophil numbers that is reduced by reconstitution with WT, but not IL-6?/?, mast cells. While IL-6 diminishes neutrophilia in mast cell-deficient mice, TGF?1 is ineffective, suggesting that these effects were mast cell dependent. Taken together, our findings establish a novel pathway through which TGF?1, likely derived from resident Tregs, controls the severity and magnitude of early innate inflammation by promoting IL-6 from mast cells. äTGF?1 limits the onset of innate lung inflammation by promoting mast c(epmc).pdf DeepDyve Pubget Overpricing