ArticleThe Journal of allergy and clinical immunology2013
Diminished allergic disease in patients with STAT3 mutations reveals a role for STAT3 signaling in mast cell degranulation.
Article in The Journal of allergy and clinical immunology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 68 papers, 1 of them a synthesis that pooled it.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
68 citing papers in PubMed, 1 synthesis or guideline pooled it, 125 citations in OpenAlex.
- A meta-analysis of the traditional herb Zicao and its active components for atopic dermatitis.Frontiers in pharmacology · 2025Pooled it
- Autosomal recessive phosphoglucomutase 3 (PGM3) mutations link glycosylation defects to atopy, immune deficiency, autoimmunity, and neurocognitive impairment.The Journal of allergy and clinical immunology · 2014Trial
- Clinical features, genetics, treatment, and long-term outcomes of STAT3 hyper-IgE syndrome: Single-center cohort analysis.The Journal of allergy and clinical immunology · 2026Observational
- DOCK8 and STAT3 cooperate to restrain IgE-inducing T follicular helper cells.The Journal of experimental medicine · 2026Article
- STAT3 haploinsufficiency is associated with autosomal dominant hyper-IgE syndrome.Science advances · 2025Article
- Hyper IgE Syndrome: Bridging the Gap Between Immunodeficiency, Atopy, and Allergic Diseases.Current allergy and asthma reports · 2025Review
- Understanding and Managing Hyper IgE Syndromes.ImmunoTargets and therapy · 2025Review
- The genetics of hyper IgE syndromes.Frontiers in immunology · 2025Review
- Kushe Tincture Ameliorates DNCB-Induced Atopic Dermatitis by Affecting NF-Kb/JAK-STAT3 Pathway: Bioinformatics Analysis and Animal Experiment Verification.Journal of inflammation research · 2025Article
- Hyper-IgE Syndrome: A Case Report with Insights from Bioinformatics Analysis of Key Pathways and Genes.Infection and drug resistance · 2025Article
- Pathophysiology of Congenital High Production of IgE and Its Consequences: A Narrative Review Uncovering a Neglected Setting of Disorders.Life (Basel, Switzerland) · 2024Review
- IL-4-STAT6 axis amplifies histamine-induced vascular endothelial dysfunction and hypovolemic shock.The Journal of allergy and clinical immunology · 2024Article
- TThe Journal of allergy and clinical immunology · 2024Review
- Insights into the pathogenesis of allergic disease from dedicator of cytokinesis 8 deficiency.Current opinion in immunology · 2023Review
- Novel mediator in anaphylaxis: decreased levels of miR-375-3p in serum and within extracellular vesicles of patients.Frontiers in immunology · 2023Article
- Review
- Diagnostic Challenges in Patients with Inborn Errors of Immunity with Different Manifestations of Immune Dysregulation.Journal of clinical medicine · 2022Review
- Interleukin-18 Receptor α Modulates the T Cell Response in Food Allergy.Allergy, asthma & immunology research · 2022Article
- Profound differences in IgE and IgG recognition of micro-arrayed allergens in hyper-IgE syndromes.Allergy · 2022Article
- Allergic manifestations of inborn errors of immunity and their impact on the diagnosis: A worldwide study.The World Allergy Organization journal · 2022Article
8 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issuedNelson, Celeste G [added]
Authors and funding
19 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundSevere atopic conditions associated with elevated serum IgE are heterogeneous with few known causes. Nearly every patient with autosomal-dominant hyper-IgE syndrome (AD-HIES) due to signal transducer and activator of transcription 3 (STAT3) mutations has a history of eczematous dermatitis and elevated IgE; however, clinical atopy has never been systematically studied.
objectiveUnderstanding of genetic determinants of allergic disease may lead to novel therapies in controlling allergic disease.
methodsWe conducted clinical evaluation of the rates of food allergies and anaphylaxis in patients with AD-HIES, a cohort of patients with no STAT3 mutation but with similar histories of elevated IgE and atopic dermatitis, and healthy volunteers with no history of atopy. Morphine skin prick testing, ImmunoCAP assays for allergen-specific IgE, and basophil activation were measured. A model of systemic anaphylaxis was studied in transgenic mice carrying an AD-HIES mutation. STAT3 was silenced in LAD2 and primary human mast cells to study the role of STAT3 in signaling and degranulation after IgE cross-linking.
resultsFood allergies and anaphylaxis were markedly diminished in patients with AD-HIES compared with a cohort of patients with no STAT3 mutation but with similar histories of elevated IgE and atopic dermatitis. Morphine skin prick testing and basophil activation were diminished in patients with AD-HIES, whereas mice carrying an AD-HIES mutation were hyporesponsive to systemic anaphylaxis models. Rapid mast cell STAT3 serine727 phosphorylation was noted after IgE cross-linking, and inhibition of STAT3 signaling in mast cells lead to impaired FcεRI-mediated proximal and distal signaling, as well as reduced degranulation.
conclusionThis study serves as an example for how mutations in specific atopic pathways can lead to discrete allergic phenotypes, encompassing increased risk of some phenotypes but a relative protection from others.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.