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10.1371/journal.pone.0131236

http://scihub22266oqcxt.onion/10.1371/journal.pone.0131236
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suck abstract from ncbi


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pmid26135595      PLoS+One 2015 ; 10 (7): ä
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  • ?? 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 FMC; Shore SA
  • PLoS One 2015[]; 10 (7): ä PMID26135595show 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.
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