Changing the threshold-Signals and mechanisms of mast cell priming

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F68378050%3A_____%2F18%3A00494578" target="_blank" >RIV/68378050:_____/18:00494578 - isvavai.cz</a>

Výsledek na webu

<a href="http://dx.doi.org/10.1111/imr.12625" target="_blank" >http://dx.doi.org/10.1111/imr.12625</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1111/imr.12625" target="_blank" >10.1111/imr.12625</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Changing the threshold-Signals and mechanisms of mast cell priming

Popis výsledku v původním jazyce

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.

Název v anglickém jazyce

Changing the threshold-Signals and mechanisms of mast cell priming

Popis výsledku anglicky

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.

Druh

J_imp - Článek v periodiku v databázi Web of Science

CEP obor

—

OECD FORD obor

30200 - Clinical medicine

Projekt

Výsledek vznikl pri realizaci vícero projektů. Více informací v záložce Projekty.

Návaznosti

P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)

Rok uplatnění

2018

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

Immunological Reviews

ISSN

0105-2896

e-ISSN

—

Svazek periodika

282

Číslo periodika v rámci svazku

1

Stát vydavatele periodika

GB - Spojené království Velké Británie a Severního Irska

Počet stran výsledku

14

Strana od-do

73-86

Kód UT WoS článku

000424876400006

EID výsledku v databázi Scopus

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