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10.1155/2016/6591703

http://scihub22266oqcxt.onion/10.1155/2016/6591703
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suck abstract from ncbi


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pmid27143818      Mediators+Inflamm 2016 ; 2016 (ä): ä
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  • Epigenetic Control of Macrophage Polarisation and Soluble Mediator Gene Expression during Inflammation #MMPMID27143818
  • Kapellos TS; Iqbal AJ
  • Mediators Inflamm 2016[]; 2016 (ä): ä PMID27143818show ga
  • Macrophages function as sentinel cells, which constantly monitor the host environment for infection or injury. Macrophages have been shown to exhibit a spectrum of activated phenotypes, which can often be categorised under the M1/M2 paradigm. M1 macrophages secrete proinflammatory cytokines and chemokines, such as TNF-?, IL-6, IL-12, CCL4, and CXCL10, and induce phagocytosis and oxidative dependent killing mechanisms. In contrast, M2 macrophages support wound healing and resolution of inflammation. In the past decade, interest has grown in understanding the mechanisms involved in regulating macrophage activation. In particular, epigenetic control of M1 or M2 activation states has been shown to rely on posttranslational modifications of histone proteins adjacent to inflammatory-related genes. Changes in methylation and acetylation of histones by methyltransferases, demethylases, acetyltransferases, and deacetylases can all impact how macrophage phenotypes are generated. In this review, we summarise the latest advances in the field of epigenetic regulation of macrophage polarisation to M1 or M2 states, with particular focus on the cytokine and chemokine profiles associated with these phenotypes.
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