Premium
Changing the threshold—Signals and mechanisms of mast cell priming
Author(s) -
Halova Ivana,
Rönnberg Elin,
Draberova Lubica,
Vliagoftis Harissios,
Nilsson Gunnar P.,
Draber Petr
Publication year - 2018
Publication title -
immunological reviews
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.839
H-Index - 223
eISSN - 1600-065X
pISSN - 0105-2896
DOI - 10.1111/imr.12625
Subject(s) - degranulation , mast cell , cytokine , immunology , immunoglobulin e , priming (agriculture) , biology , chemokine , microbiology and biotechnology , receptor , inflammation , antibody , biochemistry , botany , germination
Summary 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 E 2 , 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.