Positive and Negative Signals in Mast Cell Activation

Bulfone–Paus∥, Silvia; Nilsson, Gunnar; Dráber, Petr; Blank, Ulrich; Levi‐Schaffer, Francesca

doi:10.1016/j.it.2017.01.008

Cited by 118 publications

(112 citation statements)

References 91 publications

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“…Several types of receptors with immunoreceptor tyrosine‐based inhibitory motifs (ITIMs) have been identified to be important inhibitory regulators of FcεRI‐mediated mast cell reactivity, including FcγRIIB/CD32, CD200R, and several Ig‐like receptors . Other receptor families, including tetraspanins (CD9, CD63, CD81, and CD151) and the CD300R‐family, can mediate either activating or inhibitory signals . Thus, there is an intricate network of adapter proteins and receptors that can either increase or inhibit the FcεRI‐mediated signaling and thereby regulate the release of mediators.…”

Section: Introductionmentioning

confidence: 99%

Changing the threshold—Signals and mechanisms of mast cell priming

Hálová

Rönnberg

Dráberová

et al. 2018

Immunological Reviews

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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 , 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.

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Section: Introductionmentioning

confidence: 99%

Changing the threshold—Signals and mechanisms of mast cell priming

Hálová

Rönnberg

Dráberová

et al. 2018

Immunological Reviews

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“…Cytokines, including TNFα, IL‐33, can activate mast cells while IL‐10 and TGFβ can antagonize mast cell activation . Mast cells are also a source of cytokines.…”

Section: Itch Mediators and Receptors With Links To Mast Cells And Bamentioning

confidence: 99%

“…Concentration and binding affinity of allergens to the Fc epsilon receptor I (FcεRI), for example, skew mast cells toward a general secretion pattern of predominantly chemokines or cytokines, respectively. Furthermore, human CD300 receptor family member activation can lead to secretion of cytokines (CD300c) or inhibition of cytokine release (CD300a) . Also classical pro‐inflammatory mediators such as lipopolysaccharide directly release cytokines from mast cells, in this case via Toll‐like receptor (TLR)‐mediated release of TNFα, IL‐4 to ‐6, and IL‐13 .…”

Section: Itch Mediators and Receptors With Links To Mast Cells And Bamentioning

confidence: 99%

Role of mast cells and basophils in pruritus

Steinhoff

Buddenkotte

Lerner

2018

Immunological Reviews

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To protect our body systems, there is a constant interactive conversation between the skin nervous and immune system. Important elements of this conversation in the skin include mast cells, basophils, and sensory nerve fibers. These cells employ a vast array of sensors that detect danger and react accordingly. This reaction, summarized as neurogenic inflammation, manifests at the conscious level as sensations including pain and itch. Here we provide a perspective on the blossoming knowledge that is illuminating connections between mast cells, basophils, and sensory nerve fibers in the mediation of itch. We discuss established mediators and receptors, in particular cytokine and neuropeptide pathways, upstream proteases, and proteinase-activated receptors, and the emerging role of mas-related G-protein-coupled receptors in itch.

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“…In the last years, these events have been extensively studied and reviewed in the literature (98–104). However, given the complexity of these processes, here we present only a brief overview of the current state of affairs, focusing primarily on FcεRI.…”

Section: Cells and Molecules Involved In Food-induced Anaphylaxismentioning

confidence: 99%

Multifactorial Modulation of Food-Induced Anaphylaxis

et al. 2017

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Prevalence of food-induced anaphylaxis increases progressively and occurs in an unpredictable manner, seriously affecting the quality of life of patients. Intrinsic factors including age, physiological, and genetic features of the patient as well as extrinsic factors such as the intake of drugs and exposure to environmental agents modulate this disorder. It has been proven that diseases, such as mastocytosis, defects in HLA, or filaggrin genes, increase the risk of severe allergic episodes. Certain allergen families such as storage proteins, lipid transfer proteins, or parvalbumins have also been linked to anaphylaxis. Environmental factors such as inhaled allergens or sensitization through the skin can exacerbate or trigger acute anaphylaxis. Moreover, the effect of dietary habits such as the early introduction of certain foods in the diet, and the advantage of the breastfeeding remain as yet unresolved. Interaction of allergens with the intestinal cell barrier together with a set of effector cells represents the primary pathways of food-induced anaphylaxis. After an antigen cross-links the IgEs on the membrane of effector cells, a complex intracellular signaling cascade is initiated, which leads cells to release preformed mediators stored in their granules that are responsible for the acute symptoms of anaphylaxis. Afterward, they can also rapidly synthesize lipid compounds such as prostaglandins or leukotrienes. Cytokines or chemokines are also released, leading to the recruitment and activation of immune cells in the inflammatory microenvironment. Multiple factors that affect food-induced anaphylaxis are discussed in this review, paying special attention to dietary habits and environmental and genetic conditions.

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Positive and Negative Signals in Mast Cell Activation

Cited by 118 publications

References 91 publications

Changing the threshold—Signals and mechanisms of mast cell priming

Changing the threshold—Signals and mechanisms of mast cell priming

Role of mast cells and basophils in pruritus

Multifactorial Modulation of Food-Induced Anaphylaxis

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