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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 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\26927798 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       J+Immunol 2016 ; 196 (8 ): 3227-31 Nephropedia Template TP {{tp|p=26927798 |t=2016. Cutting Edge: CLEC5A Mediates Macrophage Function and Chronic Obstructive Pulmonary Disease Pathologies |pdf=|usr=}}{{26927798 }} gab.com Text Cutting Edge: CLEC5A Mediates Macrophage Function and Chronic Obstructive Pulmonary Disease Pathologies 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), as well as in human smokers. We also show that CLEC5A-mediated activation of macrophages enhanced cytokine elaboration alone, as well as in combination with LPS or GM-CSF in CS-exposed mice. Furthermore, usingClec5a-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 Cutting Edge: CLEC5A Mediates Macrophage Function and Chronic Obstructive Pulmonary Disease Pathologies ????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> Cutting Edge: CLEC5A Mediates Macrophage Function and Chronic Obstructive Pulmonary Disease Pathologies #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 PMID26927798 show 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), as well as in human smokers. We also show that CLEC5A-mediated activation of macrophages enhanced cytokine elaboration alone, as well as in combination with LPS or GM-CSF in CS-exposed mice. Furthermore, usingClec5a-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. |Animals [MESH] |Bronchoalveolar Lavage Fluid/cytology [MESH] |Cells, Cultured [MESH] |Cytokines/metabolism [MESH] |Disease Models, Animal [MESH] |Granulocyte-Macrophage Colony-Stimulating Factor/pharmacology [MESH] |Inflammation/immunology [MESH] |Lectins, C-Type/genetics/*immunology [MESH] |Lipopolysaccharides/adverse effects [MESH] |Lung/pathology [MESH] |Macrophage Activation/*immunology [MESH] |Macrophages, Alveolar/*immunology [MESH] |Mice [MESH] |Mice, Inbred C57BL [MESH] |Mice, Knockout [MESH] |Pulmonary Disease, Chronic Obstructive/*immunology/pathology [MESH] |Receptors, Cell Surface/genetics/*immunology [MESH]Cutting Edge: CLEC5A Mediates Macrophage Function and Chronic Obstruct(epmc).pdf DeepDyve Pubget Overpricing