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10.1371/journal.pone.0131236 http://scihub22266oqcxt.onion/10.1371/journal.pone.0131236 C4489797!4489797 !26135595     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26135595 &cmd=llinks): Failed to open stream: HTTP request failed! 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T Cells Are Required for M2 Macrophage Polarization and Resolution of Ozone-Induced Pulmonary Inflammation in Mice |pdf=|usr=}}{{26135595 }} gab.com Text T Cells Are Required for M2 Macrophage Polarization and Resolution of Ozone-Induced Pulmonary Inflammation in Mice JO: PLoS One http://www.kidney.de/pget.php?&tw=1&pmid=26135595 #FOAvip We examined the role of ?? T cells in the induction of alternatively activated M2 macrophages and the resolution of inflammation after ozone exposure. Wildtype (WT) mice and mice deficient in ?? T cells (TCR?-/- mice) were exposed to air or to ozone (0.3 ppm for up to 72h) and euthanized immediately or 1, 3, or 5 days after cessation of exposure. In WT mice, M2 macrophages accumulated in the lungs over the course of ozone exposure. Pulmonary mRNA abundance of the M2 genes, Arg1, Retnla, and Clec10a, also increased after ozone. In contrast, no evidence of M2 polarization was observed in TCR?-/- mice. WT but not TCR?-/- mice expressed the M2c polarizing cytokine, IL-17A, after ozone exposure and WT mice treated with an IL-17A neutralizing antibody exhibited attenuated ozone-induced M2 gene expression. In WT mice, ozone-induced increases in bronchoalveolar lavage neutrophils and macrophages resolved quickly after cessation of ozone exposure returning to air exposed levels within 3 days. However, lack of M2 macrophages in TCR?-/- mice was associated with delayed clearance of inflammatory cells after cessation of ozone and increased accumulation of apoptotic macrophages in the lungs. Delayed restoration of normal lung architecture was also observed in TCR?-/- mice. In summary, our data indicate that ?? T cells are required for the resolution of ozone-induced inflammation, likely because ?? T cells, through their secretion of IL-17A, contribute to changes in macrophage polarization that promote clearance of apoptotic cells. Twit Text FOAVip T Cells Are Required for M2 Macrophage Polarization and Resolution of Ozone-Induced Pulmonary Inflammation in Mice ????PLoS One http://www.kidney.de/pget.php?&tw=1&pmid=26135595 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26135595 #FOAvip English Wikipedia <ref>{{Cite pmid|26135595 }}</ref> ?? T Cells Are Required for M2 Macrophage Polarization and Resolution of Ozone-Induced Pulmonary Inflammation in Mice #MMPMID26135595 Mathews JA ; Kasahara DI ; Ribeiro L ; Wurmbrand AP ; Ninin FM ; Shore SA PLoS One 2015[]; 10 (7 ): e0131236 PMID26135595 show ga We examined the role of ?? T cells in the induction of alternatively activated M2 macrophages and the resolution of inflammation after ozone exposure. Wildtype (WT) mice and mice deficient in ?? T cells (TCR?-/- mice) were exposed to air or to ozone (0.3 ppm for up to 72h) and euthanized immediately or 1, 3, or 5 days after cessation of exposure. In WT mice, M2 macrophages accumulated in the lungs over the course of ozone exposure. Pulmonary mRNA abundance of the M2 genes, Arg1, Retnla, and Clec10a, also increased after ozone. In contrast, no evidence of M2 polarization was observed in TCR?-/- mice. WT but not TCR?-/- mice expressed the M2c polarizing cytokine, IL-17A, after ozone exposure and WT mice treated with an IL-17A neutralizing antibody exhibited attenuated ozone-induced M2 gene expression. In WT mice, ozone-induced increases in bronchoalveolar lavage neutrophils and macrophages resolved quickly after cessation of ozone exposure returning to air exposed levels within 3 days. However, lack of M2 macrophages in TCR?-/- mice was associated with delayed clearance of inflammatory cells after cessation of ozone and increased accumulation of apoptotic macrophages in the lungs. Delayed restoration of normal lung architecture was also observed in TCR?-/- mice. In summary, our data indicate that ?? T cells are required for the resolution of ozone-induced inflammation, likely because ?? T cells, through their secretion of IL-17A, contribute to changes in macrophage polarization that promote clearance of apoptotic cells. |Animals [MESH] |Antibodies, Neutralizing/pharmacology [MESH] |Apoptosis/immunology [MESH] |Arginase/genetics/immunology [MESH] |Bronchoalveolar Lavage Fluid/chemistry/cytology [MESH] |Cell Movement/drug effects [MESH] |Gene Expression Regulation [MESH] |Intercellular Signaling Peptides and Proteins/genetics/immunology [MESH] |Interleukin-17/antagonists & inhibitors/genetics/immunology [MESH] |Lectins, C-Type/genetics/immunology [MESH] |Lung/drug effects/*immunology/pathology [MESH] |Macrophage Activation/drug effects [MESH] |Macrophages/drug effects/*immunology/pathology [MESH] |Male [MESH] |Mice [MESH] |Mice, Knockout [MESH] |Neutrophils/drug effects/immunology/pathology [MESH] |Ozone/*toxicity [MESH] |Pneumonia/chemically induced/genetics/*immunology/pathology [MESH] |Receptors, Antigen, T-Cell, gamma-delta/deficiency/genetics/*immunology [MESH]?? T Cells Are Required for M2 Macrophage Polarization and Resolution (epmc).pdf DeepDyve Pubget Overpricing