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- W2888895595 abstract "Abstract IL‐33 is an IL ‐1‐related cytokine that can act as an alarmin when released from necrotic cells. Once released, it can target various immune cells including mast cells, innate lymphoid cells and T cells to elicit a Th2‐like immune response. We show here that bone marrow‐derived mast cells produce IL ‐13, IL ‐6, TNF , GM ‐ CSF , CCL 3 and CCL 4 in response to IL ‐33 stimulation. Inhibition of the p38 MAPK, or inhibition or knockout of its downstream kinases MK 2 and MK 3, blocked the production of these cytokines in response to IL ‐33. The mechanism downstream of MK 2/3 was cytokine specific; however, MK 2 and MK3 were able to regulate TNF and GM ‐ CSF mRNA stability. Previous studies in macrophages have shown that MK 2 regulates mRNA stability via phosphorylation of the RNA ‐binding protein TTP (Zfp36). The regulation of cytokine production in mast cells was, however, independent of TTP . MK 2/3 were able to phosphorylate the TTP ‐related protein Brf1 (Zfp36 l1) in IL ‐33‐stimulated mast cells, suggesting a mechanism by which MK 2/3 might control mRNA stability in these cells. In line with its ability to regulate in vitro IL ‐33‐stimulated cytokine production, double knockout of MK 2 and 3 in mice prevented neutrophil recruitment following intraperitoneal injection of IL ‐33." @default.
- W2888895595 created "2018-09-07" @default.
- W2888895595 creator A5017570232 @default.
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- W2888895595 date "2018-10-19" @default.
- W2888895595 modified "2023-10-14" @default.
- W2888895595 title "<scp>IL</scp>‐33 regulates cytokine production and neutrophil recruitment via the p38 <scp>MAPK</scp>‐activated kinases <scp>MK</scp>2/3" @default.
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- W2888895595 doi "https://doi.org/10.1111/imcb.12200" @default.
- W2888895595 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6378613" @default.
- W2888895595 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/30171775" @default.
- W2888895595 hasPublicationYear "2018" @default.
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