Tuning IgE: IgE-Associating Molecules and Their Effects on IgE-Dependent Mast Cell Reactions

Ando, Tomoaki; Kitaura, Jiro

doi:10.3390/cells10071697

Cited by 24 publications

(20 citation statements)

References 144 publications

(231 reference statements)

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“…Mast cell activation can occur following many triggers and via a plethora of cell surface receptors, including receptors for IgE, IgG, complement, cytokines, growth factors, stem cell factor, and neuropeptides (beyond the scope of this review) [ 4 , 11 , 33 ]. The prototypic IgE-mediated activation ( Figure 1 ) occurs when allergen specific IgE is bound by a multivalent allergen and interacts with the high affinity receptor for immunoglobulin E (FcεR1) carried on their surfaces [ 44 , 45 ]. The high affinity receptor for IgE has a heterotetrametric structure, comprising an α-chain (binds IgE), a β-chain (plays a key role in signal transduction), and two γ-chains (that initiate signaling post-activation) [ 45 ].…”

Section: Brief Overview Of Mast Cell Biologymentioning

confidence: 99%

“…The prototypic IgE-mediated activation ( Figure 1 ) occurs when allergen specific IgE is bound by a multivalent allergen and interacts with the high affinity receptor for immunoglobulin E (FcεR1) carried on their surfaces [ 44 , 45 ]. The high affinity receptor for IgE has a heterotetrametric structure, comprising an α-chain (binds IgE), a β-chain (plays a key role in signal transduction), and two γ-chains (that initiate signaling post-activation) [ 45 ]. This process activates a downstream signaling cascade (summarized in Figure 1 ) involving immunoreceptor tyrosine-based activation motifs (ITAMS) associated with the β- and γ-chains.…”

Section: Brief Overview Of Mast Cell Biologymentioning

confidence: 99%

“…Some pivotal cell surface receptors include those for cytokines (IL-33, IL-12, IL-10, interferon gamma/IFNγ), chemokines (CCR1-CCR7, CXCR1-6), complement (C3a/C5a, CR1-5), Toll-like receptors (TLR 1-6), histamine, prostaglandin, stem cell factor, and IgE [ 4 ]. Descriptions of these receptors and their functions are beyond the scope of this review [ 4 , 33 , 45 , 53 ].…”

Section: Brief Overview Of Mast Cell Biologymentioning

confidence: 99%

See 2 more Smart Citations

Mastocytosis and Mast Cell Activation Disorders: Clearing the Air

Jackson

Pratt

Rupprecht

et al. 2021

IJMS

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Mast cells are derived from hematopoietic stem cell precursors and are essential to the genesis and manifestations of the allergic response. Activation of these cells by allergens leads to degranulation and elaboration of inflammatory mediators, responsible for regulating the acute dramatic inflammatory response seen. Mast cells have also been incriminated in such diverse disorders as malignancy, arthritis, coronary artery disease, and osteoporosis. There has been a recent explosion in our understanding of the mast cell and the associated clinical conditions that affect this cell type. Some mast cell disorders are associated with specific genetic mutations (such as the D816V gain-of-function mutation) with resultant clonal disease. Such disorders include cutaneous mastocytosis, systemic mastocytosis (SM), its variants (indolent/ISM, smoldering/SSM, aggressive systemic mastocytosis/ASM) and clonal (or monoclonal) mast cell activation disorders or syndromes (CMCAS/MMAS). Besides clonal mast cell activations disorders/CMCAS (also referred to as monoclonal mast cell activation syndromes/MMAS), mast cell activation can also occur secondary to allergic, inflammatory, or paraneoplastic disease. Some disorders are idiopathic as their molecular pathogenesis and evolution are unclear. A genetic disorder, referred to as hereditary alpha-tryptasemia (HαT) has also been described recently. This condition has been shown to be associated with increased severity of allergic and anaphylactic reactions and may interact variably with primary and secondary mast cell disease, resulting in complex combined disorders. The role of this review is to clarify the classification of mast cell disorders, point to molecular aspects of mast cell signaling, elucidate underlying genetic defects, and provide approaches to targeted therapies that may benefit such patients.

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Section: Brief Overview Of Mast Cell Biologymentioning

confidence: 99%

Section: Brief Overview Of Mast Cell Biologymentioning

confidence: 99%

Section: Brief Overview Of Mast Cell Biologymentioning

confidence: 99%

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Mastocytosis and Mast Cell Activation Disorders: Clearing the Air

Jackson

Pratt

Rupprecht

et al. 2021

IJMS

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“… 53 , 55 , 56 Anti-IgE therapy may be effective in this regard, considering the effect on mast cells and basophils production and activation. 57 , 58 Actually, eosinophils may also have a direct role in COVID-19-related inflammation. 59 Indeed, during the first phases of respiratory infections, an active migration of circulating eosinophils from the peripheral blood to target tissues can occur, and eosinophils are known to perform some antiviral functions.…”

Section: Impact Of Anti-th2 Therapy On Covid-19: Potential Mechanismsmentioning

confidence: 99%

Impact of Anti-Type 2 Inflammation Biologic Therapy on COVID-19 Clinical Course and Outcome

Poddighe¹,

Kovzel²

2021

JIR

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SARS-CoV-2 pandemic had a general and deep impact on the clinical management of chronic diseases, including respiratory and allergic disorders. At the beginning of the pandemic, one of the main concerns was the potential impact of immunosuppressive/immunomodulatory drugs on COVID-19 clinical course. In this review, we aim to summarize and analyze the available clinical evidence from patients treated with anti-type 2 inflammation biologics (including anti-IgE, anti-IL-5 and anti-IL-4 agents), who developed COVID-19. Overall, the treatment with anti-Th2 biologics can be considered safe during COVID-19. It does not worsen the clinical course and outcome of COVID-19, and it may be actually protective somehow from developing severe forms. Moreover, patients treated with these biological agents do not seem to be more prone to get infected by SARS-CoV-2.

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“…According to the reports describing cross-talk and mutual regulation between β-AR and TGF-β signaling, 16 we wonder that whether β-AR contributes to TGF-β activation and regulates cardiac hypertrophy via activation of the cAMP-PKA pathway in cardiomyocytes? Additionally, previous studies have suggested that FcεR2, the low affinity IgE receptor, may contribute to the production of chemokines, 17 that have also been shown to function directly in cardiac remodeling. 18 Therefore, we speculate that elevated IgE induces the expression of FcεR2 in cardiomyocytes and then activates the chemokine-related pathway.…”

mentioning

confidence: 99%

IgE and TGF-β Signaling: From Immune to Cardiac Remodeling

Cao¹,

Xiao²,

He³

et al. 2021

JIR

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Cardiac remodeling is accompanied by cardiac hypertrophy, fibrosis, and dysfunction, eventually leading to heart failure (HF). However, the molecular mechanisms involved in cardiac remodeling are complicated, especially the association with immune. Immunoglobulin E (IgE) is a class of immunoglobulins involved in immune response to specific allergens. Recently, Zhao et al characterized a novel specific role of IgE and its high affinity receptor (FcεR1) in directly promoting pathological myocardial remodeling and cardiac dysfunction. Additionally, upon blocking IgE-FcεR1 signaling using FcεR1 genetic depletion or by administrating the anti-IgE monoclonal antibody omalizumab (Oma) in mice, they observed that cardiac hypertrophy and cardiac interstitial fibrosis induced by angiotensin II (Ang II) or transverse aortic constriction (TAC) were significantly suppressed. In contrast, IgE administration alone can aggravate pathological cardiac remodeling and dysfunction. RNA-seq and downstream analysis indicated that TGF-β was the common pathway and the most pivotal mediator in IgE-FcεR1-induced cardiac remodeling and dysfunction. Furthermore, the administration of a TGF-β inhibitor could ameliorate cardiac remodeling and improve cardiac function. Therefore, these findings suggest that IgE-FcεR1 maybe promising therapeutic targets for cardiac remodeling and provide an experimental basis for the use of omalizumab for HF patients combined with high serum IgE levels or allergic diseases.

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Tuning IgE: IgE-Associating Molecules and Their Effects on IgE-Dependent Mast Cell Reactions

Cited by 24 publications

References 144 publications

Mastocytosis and Mast Cell Activation Disorders: Clearing the Air

Mastocytosis and Mast Cell Activation Disorders: Clearing the Air

Impact of Anti-Type 2 Inflammation Biologic Therapy on COVID-19 Clinical Course and Outcome

IgE and TGF-β Signaling: From Immune to Cardiac Remodeling

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