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Article

Neutrophil hyperresponsiveness contributes to lung pathology in STAT3V463Δ mice.

Journal of immunology (Baltimore, Md. : 1950) - 9 Feb 2026

Brewer Killian Zane, Stone Madeline, Motamed Rachael L, Walde Ryan, Spadafora Domenico, Audia Jonathan P, Sayner Sarah, Barrington Robert A

Abstract excerpt

Autosomal dominant hyper-IgE syndrome (AD-HIES), or Job's syndrome, is a rare primary immunodeficiency caused by dominant-negative mutations in STAT3. Patients experience recurrent pulmonary infections and chronic inflammation, leading to severe complications and heightened mortality risk. To investigate whether neutrophil-intrinsic dysfunction contributes to lung pathology in AD-HIES, we used a murine model...

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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

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Source

Identifiers

PMID: 41764721
DOI: 10.1093/jimmun/vkaf373

Genes

STAT3

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026.

Related research

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Research trail→

Click a neighbor to travelStep 1 · 12 closest

Neutrophil hyperresponsiveness contributes to lung pathology in STAT3V463Δ mice.PMID 41764721Read ↗

STAT3 mutation-associated airway epithelial defects in Job syndrome.Semantic proximity Read ↗

Hyper-IgE Syndromes and the Lung.Semantic proximity Read ↗

Dysregulated Airway Host Defense in Hyper IgE Syndrome due to STAT3 MutationsSemantic proximity Read ↗

Intermediate phenotypes in patients with autosomal dominant hyper-IgE syndrome caused by somatic mosaicism.Semantic proximity Read ↗

STAT3-Dependent Regulation of CFTR and Ciliogenesis Is Essential for Mucociliary Clearance and Innate Airway Defense in Hyper-IgE Syndrome.Semantic proximity Read ↗

Pathogenesis of hyper IgE syndrome.Semantic proximity Read ↗

Dominant-negative mutations in human IL6ST underlie hyper-IgE syndrome.Semantic proximity Read ↗

Hyper IgE syndrome: an update on clinical aspects and the role of signal transducer and activator of transcription 3.Semantic proximity Read ↗

A mouse model of HIES reveals pro- and anti-inflammatory functions of STAT3.Semantic proximity Read ↗

STAT3 regulates NK and NKT cell differentiation through C-X3-C motif chemokine receptor 1 (CX3CR1) in hyper-IgE syndrome.Semantic proximity Read ↗

Defects in Jak-STAT-mediated cytokine signals cause hyper-IgE syndrome: lessons from a primary immunodeficiency.Semantic proximity Read ↗

Autosomal dominant STAT3 deficiency and hyper-IgE syndrome: molecular, cellular, and clinical features from a French national survey.Semantic proximity Read ↗

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