Changing the threshold-Signals and mechanisms of mast cell priming
Language English Country England, Great Britain Media print
Document type Journal Article, Research Support, Non-U.S. Gov't, Review
PubMed
29431203
DOI
10.1111/imr.12625
Knihovny.cz E-resources
- Keywords
- cell priming, chemokines, cytokine receptors, cytokines, high-affinity IgE receptor, mast cell,
- MeSH
- Hypersensitivity immunology MeSH
- Chemokines metabolism MeSH
- Cytokines metabolism MeSH
- Cell Degranulation * MeSH
- Immunization MeSH
- Immunoglobulin E metabolism MeSH
- Mast Cells immunology MeSH
- Inflammation Mediators metabolism MeSH
- Receptors, IgE metabolism MeSH
- Receptors, G-Protein-Coupled metabolism MeSH
- Signal Transduction MeSH
- Toll-Like Receptors metabolism MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Review MeSH
- Names of Substances
- Chemokines MeSH
- Cytokines MeSH
- Immunoglobulin E MeSH
- Inflammation Mediators MeSH
- Receptors, IgE MeSH
- Receptors, G-Protein-Coupled MeSH
- Toll-Like Receptors MeSH
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 (FcεRIs). Aggregation of FcεRIs 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 and -33), chemokines, other agents acting through G protein-coupled receptors (adenosine, prostaglandin E2 , sphingosine-1-phosphate, and β-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.
Alberta Respiratory Center and Department of Medicine University of Alberta Edmonton AB Canada
Department of Medical Sciences Uppsala University Uppsala Sweden
References provided by Crossref.org
Simultaneous reduction of all ORMDL proteins decreases the threshold of mast cell activation
Mast Cell Migration and Chemotaxis Assayed by Microscopy
