The Emerging Picture of Mast Cell Activation: The Complex Regulatory Network of High-Affinity Receptor for Immunoglobulin E Signaling

Suzuki, Ryo

doi:10.1248/bpb.b17-00465

Cited by 9 publications

(12 citation statements)

References 44 publications

(33 reference statements)

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“…52,53 FcεRI is a tetramer consisting of an a-chain that binds IgE, a membrane transversing tetraspanin b-chain, and a homodimeric disulfide-linked g-chain. 54,55 IgE is bound at 1:1 stoichiometry at very high affinity (K a > _ 10 10 M 21 ). Binding of low doses of monomeric IgE to FcεRI provides an MC survival signal, 56 and IgE levels affect surface expression of FcεRI.…”

Section: Receptors and Signaling Immunoglobulin Receptor Signalingmentioning

confidence: 99%

“…The core signaling pathways have been extensively reviewed elsewhere. 53,55,61 The relationships among the 2 classes of enzymes, other kinases and phosphatases that control MC function, are complex and sometimes hierarchical. Much has been learned from ''knockout'' or ''knockdown'' models, which need to be interpreted with caution because compensatory mechanisms might be turned on.…”

Section: Receptors and Signaling Immunoglobulin Receptor Signalingmentioning

confidence: 99%

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Regulation of the pleiotropic effects of tissue-resident mast cells

Huber

Cato

Ainooson

et al. 2019

Journal of Allergy and Clinical Immunology

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Mast cells (MCs), which are best known for their detrimental role in patients with allergic diseases, act in a diverse array of physiologic and pathologic functions made possible by the plurality of MC types. Their various developmental avenues and distinct sensitivity to (micro-) environmental conditions convey extensive heterogeneity, resulting in diverse functions. We briefly summarize this heterogeneity, elaborate on molecular determinants that allow MCs to communicate with their environment to fulfill their tasks, discuss the protease repertoire stored in secretory lysosomes, and consider different aspects of MC signaling. Furthermore, we describe key MC governance mechanisms (ie, the high-affinity receptor for IgE [FcεRI]), the stem cell factor receptor KIT, the IL-4 system, and both Ca 21and phosphatase-dependent mechanisms. Finally, we focus on distinct physiologic functions, such as chemotaxis, phagocytosis, host defense, and the regulation of MC functions at the mucosal barriers of the lung, gastrointestinal tract, and skin. A deeper knowledge of the pleiotropic functions of MC mediators, as well as the molecular processes of MC regulation and communication, should enable us to promote beneficial MC traits in physiology and suppress detrimental MC functions in patients with disease. (J Allergy Clin Immunol 2019;144:S31-45.)

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Section: Receptors and Signaling Immunoglobulin Receptor Signalingmentioning

confidence: 99%

Section: Receptors and Signaling Immunoglobulin Receptor Signalingmentioning

confidence: 99%

Regulation of the pleiotropic effects of tissue-resident mast cells

Huber

Cato

Ainooson

et al. 2019

Journal of Allergy and Clinical Immunology

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“…Regulatory T (Treg) cells can weaken anti-tumor immune responses, which could serve as a promising immuno-therapeutic approach for tumors [ 40 ]. The Fc epsilon RI receptor induces multiple signaling pathways that control the secretion of allergic mediators and induction of cytokine gene transcription, resulting in secretion of various molecules: IL-4, IL-5, IL-6, IL-10, IL-13, INF-gamma (interferon-gamma), and TNF-alpha (tumor necrosis factor alpha) [ 41 ]. We provide detailed information of the 20 most meaningful enrichment pathways in Table 4 .…”

Section: Resultsmentioning

confidence: 99%

“…Infection with CML has important secondary symptoms. Enrichment pathways of Qingdai putative targets involve immune and inflammatory pathways, which activate the patient’s own immune system and enhance the defence against sources of external infection, such as phagocytosis of immune cells, which plays an essential role in host defence mechanisms by enveloping and destroying infectious pathogens [ 41 ].…”

Section: Resultsmentioning

confidence: 99%

Deciphering Key Pharmacological Pathways of Qingdai Acting on Chronic Myeloid Leukemia Using a Network Pharmacology-Based Strategy

Liu

et al. 2018

Med Sci Monit

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Qingdai, a traditional Chinese medicine (TCM) used for the treatment of chronic myeloid leukemia (CML) with good efficacy, has been used in China for decades. However, due to the complexity of traditional Chinese medicinal compounds, the pharmacological mechanism of Qingdai needs further research. In this study, we investigated the pharmacological mechanisms of Qingdai in the treatment of CML using network pharmacology approaches.First, components in Qingdai that were selected by pharmacokinetic profiles and biological activity predicted putative targets based on a combination of 2D and 3D similarity measures with known ligands. Then, an interaction network of Qingdai putative targets and known therapeutic targets for the treatment of chronic myeloid leukemia was constructed. By calculating the 4 topological features (degree, betweenness, closeness, and coreness) of each node in the network, we identified the candidate Qingdai targets according to their network topological importance. The composite compounds of Qingdai and the corresponding candidate major targets were further validated by a molecular docking simulation.Seven components in Qingdai were selected and 32 candidate Qingdai targets were identified; these were more frequently involved in cytokine-cytokine receptor interaction, cell cycle, p53 signaling pathway, MAPK signaling pathway, and immune system-related pathways, which all play important roles in the progression of CML. Finally, the molecular docking simulation showed that 23 pairs of chemical components and candidate Qingdai targets had effective binding.This network-based pharmacology study suggests that Qingdai acts through the regulation of candidate targets to interfere with CML and thus regulates the occurrence and development of CML.

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“…These receptors can be classified historically as IgE-dependent and non-IgE-dependent receptors, based on their positive or negative response to immunoglobulins E (IgE) 66 . The best example of an IgE-dependent receptor is the High affinity IgE receptor (FcεRI) 67,68 . Non-IgE-dependent receptors include the recently discovered G-Protein-Coupled Receptors (GPCR) which respond to less specific agonists 63,65,[69][70][71][72] .…”

Section: Physio-pathological Effects Of Cellular Acidification In Epimentioning

confidence: 99%

Acids Can Promote the Onset and Multimorbidity of Allergic and Nonallergic Airway Diseases

Molinari¹,

Molinari²,

Nervo³

2019

Preprint

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Inflammatory allergic and nonallergic respiratory pathologies often co-exist. The root cause is not clear. This paper demonstrates that it is ascribable to protons (H+) released into cells by exogenous and endogenous acids. The hypothesis of acids as the common cause stems from two considerations: a) it has long been known that exogenous acids present in air pollutants can induce the irritation of epithelial surfaces, particularly the airways, inflammation and bronchospasm; b) according to recent articles, endogenous acids, generated in cells by phospholipases, play a key role in the biochemical mechanisms of initiation and progression of allergic responses. Therefore, the intracellular acidification and consequent Ca2+ increase, induced by protons generated by either acid pollutants or endogenous phospholipases, may be the causal mechanism of the multimorbidity of these diseases, and environmental acidity may contribute to their spread.

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The Emerging Picture of Mast Cell Activation: The Complex Regulatory Network of High-Affinity Receptor for Immunoglobulin E Signaling

Cited by 9 publications

References 44 publications

Regulation of the pleiotropic effects of tissue-resident mast cells

Regulation of the pleiotropic effects of tissue-resident mast cells

Deciphering Key Pharmacological Pathways of Qingdai Acting on Chronic Myeloid Leukemia Using a Network Pharmacology-Based Strategy

Acids Can Promote the Onset and Multimorbidity of Allergic and Nonallergic Airway Diseases

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