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Changing the threshold-Signals and mechanisms of mast cell priming
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SYSNO ASEP 0494578 Document Type J - Journal Article R&D Document Type Journal Article Subsidiary J Článek ve WOS Title Changing the threshold-Signals and mechanisms of mast cell priming Author(s) Hálová, Ivana (UMG-J) RID, ORCID
Ronnberg, E. (SE)
Dráberová, Lubica (UMG-J) RID
Vliagoftis, H. (SE)
Nilsson, G.P. (SE)
Dráber, Petr (UMG-J) RIDNumber of authors 6 Source Title Immunological Reviews. - : Wiley - ISSN 0105-2896
Roč. 282, č. 1 (2018), s. 73-86Number of pages 14 s. Language eng - English Country GB - United Kingdom Keywords cell priming ; chemokines ; cytokine receptors ; cytokines ; high-affinity IgE receptor ; mast cell Subject RIV EB - Genetics ; Molecular Biology OECD category 3.2 Clinical medicine R&D Projects GA17-20255S GA ČR - Czech Science Foundation (CSF) GA17-20915S GA ČR - Czech Science Foundation (CSF) Institutional support UMG-J - RVO:68378050 UT WOS 000424876400006 DOI 10.1111/imr.12625 Annotation Mast cells play a key role in allergy and other inflammatory diseases involving engagement of multivalent antigen with IgE bound to high-affinity IgE receptors (Fc epsilon RIs). Aggregation of Fc epsilon RIs on mast cells initiates a cascade of signaling events that eventually lead to degranulation, secretion of leukotrienes and prostaglandins, and cytokine and chemokine production contributing to the inflammatory response. Exposure to pro-inflammatory cytokines, chemokines, bacterial and viral products, as well as some other biological products and drugs, induces mast cell transition from the basal state into a primed one, which leads to enhanced response to IgE-antigen complexes. Mast cell priming changes the threshold for antigen-mediated activation by various mechanisms, depending on the priming agent used, which alone usually do not induce mast cell degranulation. In this review, we describe the priming processes induced in mast cells by various cytokines (stem cell factor, interleukins-4,6 and33), chemokines, other agents acting through G protein-coupled receptors (adenosine, prostaglandin E-2, sphingosine-1-phosphate, and beta-2-adrenergic receptor agonists), toll-like receptors, and various drugs affecting the cytoskeleton. We will review the current knowledge about the molecular mechanisms behind priming of mast cells leading to degranulation and cytokine production and discuss the biological effects of mast cell priming induced by several cytokines. Workplace Institute of Molecular Genetics Contact Nikol Škňouřilová, nikol.sknourilova@img.cas.cz, Tel.: 241 063 217 Year of Publishing 2019
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