scholarly journals Microarray-Based Allergy Diagnosis: Quo Vadis?

2021 ◽  
Vol 11 ◽  
Author(s):  
Huey-Jy Huang ◽  
Raffaela Campana ◽  
Oluwatoyin Akinfenwa ◽  
Mirela Curin ◽  
Eszter Sarzsinszky ◽  
...  
Keyword(s):  
Large Scale ◽  
Unmet Needs ◽  
Immunoglobulin E ◽  
Late Phase ◽  
Allergic Inflammation ◽  
Specific Ige ◽  
Recombinant Allergen ◽  
World Population ◽  
Allergy Diagnosis ◽  
Quo Vadis

More than 30% of the world population suffers from allergy. Allergic individuals are characterized by the production of immunoglobulin E (IgE) antibodies against innocuous environmental allergens. Upon allergen recognition IgE mediates allergen-specific immediate and late-phase allergic inflammation in different organs. The identification of the disease-causing allergens by demonstrating the presence of allergen-specific IgE is the key to precision medicine in allergy because it allows tailoring different forms of prevention and treatment according to the sensitization profiles of individual allergic patients. More than 30 years ago molecular cloning started to accelerate the identification of the disease-causing allergen molecules and enabled their production as recombinant molecules. Based on recombinant allergen molecules, molecular allergy diagnosis was introduced into clinical practice and allowed dissecting the molecular sensitization profiles of allergic patients. In 2002 it was demonstrated that microarray technology allows assembling large numbers of allergen molecules on chips for the rapid serological testing of IgE sensitizations with small volumes of serum. Since then microarrayed allergens have revolutionized research and diagnosis in allergy, but several unmet needs remain. Here we show that detection of IgE- and IgG-reactivity to a panel of respiratory allergens microarrayed onto silicon elements is more sensitive than glass-based chips. We discuss the advantages of silicon-based allergen microarrays and how this technology will allow addressing hitherto unmet needs in microarray-based allergy diagnosis. Importantly, it described how the assembly of silicon microarray elements may create different microarray formats for suiting different diagnostic applications such as quick testing of single patients, medium scale testing and fully automated large scale testing.

scholarly journals Tracing IgE-Producing Cells in Allergic Patients

Cells ◽  
2019 ◽  
Vol 8 (9) ◽  
pp. 994 ◽  
Author(s):  
Julia Eckl-Dorna ◽  
Sergio Villazala-Merino ◽  
Nicholas James Campion ◽  
Maria Byazrova ◽  
Alexander Filatov ◽  
...  
Keyword(s):  
Plasma Cells ◽  
Immunoglobulin E ◽  
Current Knowledge ◽  
Allergic Diseases ◽  
Specific Ige ◽  
Allergen Exposure ◽  
World Population ◽  
Effector Cells ◽  
Ige Receptors ◽  
Pre Treatment

Immunoglobulin E (IgE) is the key immunoglobulin in the pathogenesis of IgE associated allergic diseases affecting 30% of the world population. Recent data suggest that allergen-specific IgE levels in serum of allergic patients are sustained by two different mechanisms: inducible IgE production through allergen exposure, and continuous IgE production occurring even in the absence of allergen stimulus that maintains IgE levels. This assumption is supported by two observations. First, allergen exposure induces transient increases of systemic IgE production. Second, reduction in IgE levels upon depletion of IgE from the blood of allergic patients using immunoapheresis is only temporary and IgE levels quickly return to pre-treatment levels even in the absence of allergen exposure. Though IgE production has been observed in the peripheral blood and locally in various human tissues (e.g., nose, lung, spleen, bone marrow), the origin and main sites of IgE production in humans remain unknown. Furthermore, IgE-producing cells in humans have yet to be fully characterized. Capturing IgE-producing cells is challenging not only because current staining technologies are inadequate, but also because the cells are rare, they are difficult to discriminate from cells bearing IgE bound to IgE-receptors, and plasma cells express little IgE on their surface. However, due to the central role in mediating both the early and late phases of allergy, free IgE, IgE-bearing effector cells and IgE-producing cells are important therapeutic targets. Here, we discuss current knowledge and unanswered questions regarding IgE production in allergic patients as well as possible therapeutic approaches targeting IgE.

MOLECULAR IDENTIFICATION OF AN IMMUNOGLOBULIN E (IgE)-DEPENDENT HISTAMINE-RELEASING FACTOR

PEDIATRICS ◽  
1996 ◽  
Vol 98 (2) ◽  
pp. 324-324
Author(s):  
Scott H. Sicherer ◽  
Robert A. Wood
Keyword(s):  
Histamine Release ◽  
Recombinant Proteins ◽  
Mononuclear Cells ◽  
Immunoglobulin E ◽  
Polyclonal Antibodies ◽  
Late Phase ◽  
Allergic Inflammation ◽  
Protein Sequencing ◽  
Human Macrophage ◽  
Polymerase Chain

Purpose of the Study. The late-phase allergic response depends in part on histamine release from immunoglobulin E (IgE)-bearing basophils that collect at the site of allergic inflammation at a time when allergen has been metabolized. This phenomenon lead to the search for cytokines that can cause histamine release from basophils. Although several cytokines can cause basophil histamine release, only one histamine-releasing factor (HRF), which has been found in late-phase response fluids, causes histamine release only from basophils bearing IgE. In fact, this HRF only releases histamine from basophils bearing a particular type of IgE (termed IgE+) that is only produced by a subset of allergic individuals. This study sought to identify this HRF molecule. Methods/Results. Fifty liters of supernatant containing HRF from a human macrophage line was concentrated and the proteins were separated by electrophoresis. Protein sequencing was performed on a 23-kD band and revealed extensive homology to a mouse protein, p21. and its human homologue, p23. Both of the genes for these proteins had been previously cloned because of extensive expression in tumor cells but no function had been ascribed to them. Both recombinant proteins caused histamine release from the human basophils of a subpopulation of donors, and this release was dependent on IgE. Polyclonal antibodies to the recombinant proteins were raised and were capable of removing the biologic activity of recombinant and native HRF. RNA blot analysis and reverse transcription polymerase chain reaction indicated that the HRF mRNA was ubiquitous and found in T cells, B cells, fibroblasts, and mononuclear cells.

LncRNA MIAT Promotes Allergic Inflammation and Symptoms by Targeting MiR-10b-5p in Allergic Rhinitis Mice

2021 ◽  
Vol 35 (6) ◽  
pp. 781-789
Author(s):  
Zhiqi Ma ◽  
Haijuan Lian ◽  
Xiaoyan Lin ◽  
Yong Li
Keyword(s):  
Allergic Rhinitis ◽  
Nasal Mucosa ◽  
Th17 Cells ◽  
Immunoglobulin E ◽  
Allergic Inflammation ◽  
Specific Ige ◽  
Luciferase Reporter ◽  
Mice Model ◽  
Ige Response ◽  
The Relationship

Background Allergic rhinitis (AR) is one of the most common noninfectious respiratory diseases caused by immunoglobulin E (IgE) response. Objective The study sought to explore the relationship between lncRNA MIAT and miR-10b-5p and their interaction in the regulation of allergic phenotypes in allergic rhinitis (AR) mice. Methods A mice model of AR was constructed using ovalbumin (OVA) sensitization. AR mice were treated with miR-10b-5p agomiR and LNA mediated lncRNA MIAT. The targeting relationship between MIAT and miR-10b-5p was analyzed by the ENCORI website and dual-luciferase reporter assay. The numbers of rubbing and sneezing of mice were counted. Hematoxylin-eosin (HE) staining visualized the eosinophils infiltration in nasal mucosa tissues of mice. The percentage of Th17 cells was quantitated by flow cytometry analysis. ELISA was used to detect the levels of serum OVA-specific IgE, the Th12 cytokine IL-4, and inflammatory cytokines (IL-6, IL-17). Results MIAT was up-regulated in the nasal mucosa of AR mice, while miR-10b-5p was down-regulated. MIAT directly suppressed miR-10b-5p expression in AR mice. The numbers of rubbing and sneezing, the percentage of Th17 cells, and the levels of OVA-specific IgE, IL-4, IL-6, and IL-17 in AR mice were decreased by miR-10b-5p overexpression, which was reversed by MIAT overexpression. The eosinophils infiltration in AR mice was inhibited by miR-10b-5p overexpression, which was also reversed by MIAT overexpression. Conclusion The present study demonstrates that MIAT overexpression Promotes allergic inflammation and symptoms by activating Th17 immune response via miR-10b-5p inhibition.

THE HIGH-AFFINITY IMMUNOGLOBULIN E (IgE) RECEPTOR (FcεRI) MEDIATES IgE-DEPENDENT ALLERGEN PRESENTATION

PEDIATRICS ◽  
1996 ◽  
Vol 98 (2) ◽  
pp. 325-325
Author(s):  
Russell Hopp
Keyword(s):  
Immunoglobulin E ◽  
Late Phase ◽  
Specific Ige ◽  
Delayed Response ◽  
Target Area ◽  
Type I ◽  
Ige Receptor ◽  
High Affinity ◽  
Ige Receptors ◽  
Response Target

Low numbers of monocytes with highaffinity IgE receptors and bound-specific IgE, attracted to the late-phase response target area (skin, nose, or lungs) may be a prime cell for the initiation of further Type I immediate and Type I late-phase responses (referred to as T cell mediated, delayed response, in this paper).

scholarly journals Serum IgE Predicts Difference of Population and Allergens in Allergic Diseases: Data from Weifang City, China

2021 ◽  
Vol 2021 ◽  
pp. 1-9
Author(s):  
Zhang Xu-De ◽  
Guo Bei-Bei ◽  
Wang Xi-Juan ◽  
Li Hai-Bo ◽  
Zhang Li-Li ◽  
...  
Keyword(s):  
Immunoglobulin E ◽  
Allergic Inflammation ◽  
Allergic Diseases ◽  
Specific Ige ◽  
Serum Ige ◽  
Disease Spectrum ◽  
Positive Rate ◽  
Single Positive ◽  
Artemisia Pollen

Background. Immunoglobulin E (IgE) is the most important promoter of allergic inflammation. However, there are few systematic studies on IgE in age range, genders, disease spectrum, and time regularity. Aim. To screen the common allergens, allergen spectrum, and IgE difference between type 2 inflammatory allergic diseases and other allergic diseases in Weifang, China. Methods. A retrospective study was performed by estimating patients’ clinical data suffering from allergic diseases (urticaria, pollinosis, allergic rhinitis, atopic dermatitis, and bronchial asthma) between May 2019 and April 2020 using an allergen detection kit of Macro-Union Pharmaceutical. Results. 732 of the 1367 patients showed different antigen positive, and the positive rate was 53.5%. The most common allergens were dust mites, mixed fungi, Artemisia pollen, cat/dog dander, and cockroaches. There were 27.0% (369/1367) of the patients with single positive allergen-specific IgE (sIgE), 26.5% (363/1367) with multiple-positive IgE. The total immunoglobulin E (tIgE) levels varied with gender, age, and type of disease. There was a difference in the distribution of allergens between children and adults. A positive correlation between the serum-specific IgE and the corresponding local inhaled allergen density was observed. Conclusions. In this study, we found that type 2 inflammatory allergic diseases have higher serum IgE and a higher probability of inhaled sIgE positive. According to age, gender, and condition, serological IgE detection of allergens provides new insight into the early diagnosis and prevention of allergic diseases.

scholarly journals The role of IgE, IgG, and IgA in tolerance, sensitization, and targeted treatment of allergic disease

2021 ◽  
Author(s):  
Mohamed Shamji ◽  
Rudolf Valenta ◽  
Theodore Jardetzky ◽  
Valerie Verhasselt ◽  
Stephen Durham ◽  
...  
Keyword(s):  
Immunoglobulin E ◽  
Allergic Sensitization ◽  
Passive Immunization ◽  
Allergic Inflammation ◽  
Allergic Diseases ◽  
Immediate Release ◽  
Specific Ige ◽  
Allergen Specific Immunotherapy ◽  
Effector Cells ◽  
Iga Antibodies

Immunoglobulin E (IgE)-mediated allergy is the most common hypersensitivity disease affecting more than 30% of the population. In genetically-predisposed subjects exposure to minute quantities of allergens leads to the production of IgE antibodies which is termed allergic sensitization and mainly occurs in early childhood. Allergen-specific IgE then binds to the high (FcRI) and low affinity receptors (FcRII, also called CD23) for IgE on effector cells and antigen-presenting cells, respectively. Subsequent and repeated allergen exposure increases allergen-specific IgE levels and, by receptor cross-linking, triggers immediate release of inflammatory mediators from mast cells and basophils whereas IgE-facilitated allergen presentation perpetuates T cell-mediated allergic inflammation. Due to engagement of receptors which are highly selective for IgE even tiny amounts of allergens can induce massive inflammation. Naturally occurring allergen-specific IgG and IgA antibodies usually recognize different epitopes on allergens compared to IgE, and do not efficiently interfere with allergen-induced inflammation. However IgG and IgA antibodies to these important IgE epitopes can be induced by allergen-specific immunotherapy or by passive immunization. These will lead to competition with IgE for binding with the allergen and prevent allergic responses. Similarly, anti-IgE treatment does the same by preventing IgE from binding to its receptor on mastcells and basophils. Here we review the complex interplay of allergen-specific IgE, IgG and IgA and the corresponding cell receptors in allergic diseases and its relevance for diagnosis, treatment and prevention of allergy.

scholarly journals The role of IgE, IgG, and IgA in tolerance, sensitization, and targeted treatment of allergic disease

2021 ◽  
Author(s):  
Mohamed Shamji ◽  
Rudolf Valenta ◽  
Theodore Jardetzky ◽  
Valerie Verhasselt ◽  
Stephen Durham ◽  
...  
Keyword(s):  
Immunoglobulin E ◽  
Allergic Sensitization ◽  
Passive Immunization ◽  
Allergic Inflammation ◽  
Allergic Diseases ◽  
Immediate Release ◽  
Specific Ige ◽  
Allergen Specific Immunotherapy ◽  
Effector Cells ◽  
Iga Antibodies

Immunoglobulin E (IgE)-mediated allergy is the most common hypersensitivity disease affecting more than 30% of the population. In genetically-predisposed subjects exposure to minute quantities of allergens leads to the production of IgE antibodies which is termed allergic sensitization and mainly occurs in early childhood. Allergen-specific IgE then binds to the high (FcRI) and low affinity receptors (FcRII, also called CD23) for IgE on effector cells and antigen-presenting cells, respectively. Subsequent and repeated allergen exposure increases allergen-specific IgE levels and, by receptor cross-linking, triggers immediate release of inflammatory mediators from mast cells and basophils whereas IgE-facilitated allergen presentation perpetuates T cell-mediated allergic inflammation. Due to engagement of receptors which are highly selective for IgE even tiny amounts of allergens can induce massive inflammation. Naturally occurring allergen-specific IgG and IgA antibodies usually recognize different epitopes on allergens compared to IgE, and do not efficiently interfere with allergen-induced inflammation. However IgG and IgA antibodies to these important IgE epitopes can be induced by allergen-specific immunotherapy or by passive immunization. These will lead to competition with IgE for binding with the allergen and prevent allergic responses. Similarly, anti-IgE treatment does the same by preventing IgE from binding to its receptor on mastcells and basophils. Here we review the complex interplay of allergen-specific IgE, IgG and IgA and the corresponding cell receptors in allergic diseases and its relevance for diagnosis, treatment and prevention of allergy.

in NS

2021 ◽  
Author(s):  
Stefania Arasi ◽  
Ilenia Panasiti ◽  
Lucia Caminiti ◽  
Mariaelisabetta Conte ◽  
Sveva Castelli ◽  
...  
Keyword(s):  
Late Phase ◽  
Specific Treatment ◽  
Allergic Inflammation ◽  
Serum Levels ◽  
Specific Ige ◽  
Neurotrophin 3 ◽  
Paediatric Age ◽  
Nasal Secretions ◽  
Tailored Approach

BACKGROUND: Characterization of disease endotypes will open a new window for the treatment of allergic rhinitis (AR). Herein we provide the first attempt to identify specific AR phenotypes/endotypes and/or any biomarker/predictor for specific treatment response based on local biological parameters. METHODS: This observational study was carried out in 142 patients with seasonal AR and 20 non-allergic controls. Total IgE levels, specific IgE to 112 allergenic molecules and 92 proinflammatory and immunologic proteins were measured in both serum and nasal secretions (NS). RESULTS: We found increased values of MCPs and MMPs in adults both in NS and serum when compared with pediatric patients (p<.05). MCPs and MMPs might represent two effective predictors of chronic inflammation. CXCL9, CXCL10, CXCL11, MCPs and MMP1 showed an upward trend both in serum and NS for patients with ≥ 3 comorbidities vs non-allergic controls(p<.05). These data suggest the involvement of these chemokines in the late phase of chronic allergic inflammation in the nose. Serum levels of IL-6, IL-8 and IL-10 (p<.05) were significantly higher in patients with AR+asthma compared to patients with different comorbidities. Conversely, serum levels of neurotrophin-3 values (p<.05) were significantly higher in those with AR+eczema vs other comorbidities groups. A subgroup of patients with a nasal hypersecretory state,called “hypersecreter endotype” was characterized by paediatric age, male gender, grass pollen sensitization and distributed among persistent, mild or moderate to severe cases of AR. CONCLUSIONS: Our study sets the groundwork for an AR endotypization at molecular level, which is highly desirable to deliver a patient-tailored approach.

Immunotheraphy in Allergic Diseases

2018 ◽  
Vol 24 (11) ◽  
pp. 1174-1194
Author(s):  
Albert Roger ◽  
Maria Basagana ◽  
Aina Teniente-Serra ◽  
Nathalie Depreux ◽  
Yanina Jurgens ◽  
...  
Keyword(s):  
Specific Immunotherapy ◽  
Allergic Diseases ◽  
Specific Ige ◽  
World Population ◽  
Allergen Specific Immunotherapy ◽  
Routes Of Administration ◽  
Disease Modifying Therapy ◽  
History Of ◽  
Ige Mediated ◽  
Special Case

The prevalence of allergic diseases is increasing worldwide. It is estimated that more than 30% of the world population is now affected by one or more allergic conditions and a high proportion of this increase is in young people. The diagnosis of allergy is dependent on a history of symptoms on exposure to an allergen together with the detection of allergen-specific IgE. Accurate diagnosis of allergies opens up therapeutic options. Allergen specific immunotherapy is the only successful disease-modifying therapy for IgE-mediated allergic diseases. New therapeutic strategies have been developed or are currently under clinical trials. Besides new routes of administration, new types of allergens are being developed. The use of adjuvants may amplify the immune response towards tolerance to the antigens. In this review, we analyze different antigen-specific immunotherapies according to administration route, type of antigens and adjuvants, and we address the special case of food allergy.

scholarly journals SERPINB10 contributes to asthma by inhibiting the apoptosis of allergenic Th2 cells

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Yuqing Mo ◽  
Ling Ye ◽  
Hui Cai ◽  
Guiping Zhu ◽  
Jian Wang ◽  
...  
Keyword(s):  
T Cells ◽  
Allergic Asthma ◽  
Cd4 T Cells ◽  
Quantitative Polymerase Chain Reaction ◽  
Allergic Inflammation ◽  
Specific Ige ◽  
Th2 Cells ◽  
Th1 Cells ◽  
Th2 Response ◽  
Th1 And Th2

Abstract Background Serine peptidase inhibitor, clade B, member 10 (SERPINB10) contributes to allergic inflammation in asthma. However, its role in the T-helper type 2 (Th2) response of allergic asthma is not known. The goal of this study was to unveil the function of SERPINB10 in the Th2 response of allergic asthma and the mechanism by which SERPINB10 affects the viability of Th2 cells. Methods Th2 cytokines and serum levels of house dust mite (HDM)-specific IgE in bronchoalveolar lavage fluid were examined by ELISA in an HDM-induced asthma model. The number and apoptosis of Th1 and Th2 cells in mouse lungs were measured by flow cytometry. Naïve CD4 T cells from patients with asthma were cultured under appropriate polarizing conditions to generate Th1 and Th2 cells. SERPINB10 expression in polarized Th1 and Th2 cells was quantified by real-time reverse transcription-quantitative polymerase chain reaction. SERPINB10 expression was knocked down in human CD4 T cells with lentivirus. Results Knockdown of SERPINB10 expression significantly diminished HDM-induced Th2 cytokine secretion and level of HDM-specific IgE. After HDM exposure, SERPINB10-knockdown mice had diminished numbers of Th2 cells, but similar numbers of Th1 cells, compared with those in negative-control mice. Th2 cells of SERPINB10-knockdown mice were more susceptible to apoptosis than that of control mice. Stimulating T-cell receptors (TCRs) with anti-CD3 antibody caused upregulation of SERPINB10 expression in polarized Th2 cells, but not polarized Th1 cells. Knockdown of SERPINB10 expression resulted in fewer numbers and greater apoptosis of polarized Th2 cells. Conclusion Our results suggest that SERPINB10 may contribute to allergic inflammation and the Th2 response of asthma by inhibiting the apoptosis of Th2 cells.

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