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10.1002/eji.201545501

http://scihub22266oqcxt.onion/10.1002/eji.201545501
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C4813659!4813659!26256265
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suck abstract from ncbi


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pmid26256265      Eur+J+Immunol 2015 ; 45 (11): 3034-44
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  • Activated mast cells synthesize and release soluble ST2-a decoy receptor for IL-33 #MMPMID26256265
  • Bandara G; Beaven MA; Olivera A; Gilfillan AM; Metcalfe DD
  • Eur J Immunol 2015[Nov]; 45 (11): 3034-44 PMID26256265show ga
  • Interleukin 33 (IL-33) released from damaged cells plays a central role in allergic inflammation by acting through its membrane-bound receptor, ST2 receptor (ST2L). IL-33 activity can be neutralized by the soluble spliced variant of ST2 (sST2) which has been associated with allergic inflammation but its source is not well defined. We investigated whether mast cells (MCs) are a significant source of sST2 following activation through Fc?RI or ST2. We find that antigen and IL-33 induce substantial production and release of sST2 from human and mouse MCs in culture and do so synergistically when added together or in combination with stem cell factor. Moreover, increases in circulating sST2 during anaphylaxis in mice were dependent on the presence of MCs. Human MCs activated via Fc?RI failed to generate IL-33 and IL-33 produced by mouse bone marrow-derived MCs was retained within the cells. Therefore, Fc?RI-mediated sST2 production is independent of MC-derived IL-33 acting in an autocrine manner. These results are consistent with the conclusion that both mouse and human MCs when activated are a significant inducible source of sST2 but not IL-33 and thus have the ability to modulate the biologic impact of IL-33 produced locally by other cell types during allergic inflammation.
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