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10.1016/j.ejphar.2015.02.057

http://scihub22266oqcxt.onion/10.1016/j.ejphar.2015.02.057
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suck abstract from ncbi


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pmid25941081
      Eur+J+Pharmacol 2016 ; 778 (ä): 11-23
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  • Signal transduction and chemotaxis in mast cells #MMPMID25941081
  • Draber P ; Halova I ; Polakovicova I ; Kawakami T
  • Eur J Pharmacol 2016[May]; 778 (ä): 11-23 PMID25941081 show ga
  • Mast cells play crucial roles in both innate and adaptive arms of the immune system. Along with basophils, mast cells are essential effector cells for allergic inflammation that causes asthma, allergic rhinitis, food allergy and atopic dermatitis. Mast cells are usually increased in inflammatory sites of allergy and, upon activation, release various chemical, lipid, peptide and protein mediators of allergic reactions. Since antigen/immunoglobulin E (IgE)-mediated activation of these cells is a central event to trigger allergic reactions, innumerable studies have been conducted on how these cells are activated through cross-linking of the high-affinity IgE receptor (Fc?RI). Development of mature mast cells from their progenitor cells is under the influence of several growth factors, of which the stem cell factor (SCF) seems to be the most important. Therefore, how SCF induces mast cell development and activation via its receptor, KIT, has been studied extensively, including a cross-talk between KIT and Fc?RI signaling pathways. Although our understanding of the signaling mechanisms of the Fc?RI and KIT pathways is far from complete, pharmaceutical applications of the knowledge about these pathways are underway. This review will focus on recent progresses in Fc?RI and KIT signaling and chemotaxis.
  • |*Chemotaxis/drug effects [MESH]
  • |*Signal Transduction/drug effects [MESH]
  • |Animals [MESH]
  • |Humans [MESH]


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