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10.4049/jimmunol.1500978 http://scihub22266oqcxt.onion/10.4049/jimmunol.1500978 C4821706!4821706!26927798     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       J+Immunol 2016 ; 196 (8): 3227-31 Nephropedia Template TP {{tp|p=26927798|t=2016. CLEC5A Mediates Macrophage Function and COPD Pathologies1 |pdf=|usr=}}{{26927798}} gab.com Text CLEC5A Mediates Macrophage Function and COPD Pathologies1 JO: J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=26927798 #FOAvip Chronic Obstructive Pulmonary Disease (COPD) is a devastating disease with no effective therapies. We investigated the role of the C-type lectin receptor, CLEC5A, in macrophage activation and pulmonary pathogenesis in a mouse model of COPD. We demonstrate that CLEC5A is expressed on alveolar macrophages in mice exposed long-term to cigarette smoke (CS) and in human smokers. We also show that CLEC5A-mediated activation of macrophages enhanced cytokine elaboration alone, and in combination with LPS or GM-CSF in CS-exposed mice. Furthermore, using Clec5a-deficient mice, we demonstrate that CS-induced macrophage responsiveness is mediated by CLEC5A and CLEC5A is required for the development of inflammation, proinflammatory cytokine expression and airspace enlargement. These findings suggest a novel mechanism that promotes airway inflammation and pathologies in response to CS exposure and identifies CLEC5A as a novel target for the therapeutic control of COPD pathogenesis. Twit Text FOAVip CLEC5A Mediates Macrophage Function and COPD Pathologies1 ????J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=26927798 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26927798 #FOAvip English Wikipedia <ref>{{Cite pmid|26927798}}</ref> CLEC5A Mediates Macrophage Function and COPD Pathologies1 #MMPMID26927798 Wortham BW; Eppert BL; Flury JL; Garcia SM; Donica WR; Osterburg A; Joyce-Shaikh B; Cua DJ; Borchers MT J Immunol 2016[Apr]; 196 (8): 3227-31 PMID26927798show ga Chronic Obstructive Pulmonary Disease (COPD) is a devastating disease with no effective therapies. We investigated the role of the C-type lectin receptor, CLEC5A, in macrophage activation and pulmonary pathogenesis in a mouse model of COPD. We demonstrate that CLEC5A is expressed on alveolar macrophages in mice exposed long-term to cigarette smoke (CS) and in human smokers. We also show that CLEC5A-mediated activation of macrophages enhanced cytokine elaboration alone, and in combination with LPS or GM-CSF in CS-exposed mice. Furthermore, using Clec5a-deficient mice, we demonstrate that CS-induced macrophage responsiveness is mediated by CLEC5A and CLEC5A is required for the development of inflammation, proinflammatory cytokine expression and airspace enlargement. These findings suggest a novel mechanism that promotes airway inflammation and pathologies in response to CS exposure and identifies CLEC5A as a novel target for the therapeutic control of COPD pathogenesis. äCLEC5A Mediates Macrophage Function and COPD Pathologies1 (epmc).pdf DeepDyve Pubget Overpricing