Raras
Buscar doenças, sintomas, genes...
Síndrome de hiper IgE
ORPHA:331223CID-11 · 4A01.34DOENÇA RARA

Uma condição caracterizada por níveis elevados de IgE no sangue, inflamação da pele e infecções respiratórias.

Mantido por Agente Raras·Colaborar como especialista →

Introdução

O que você precisa saber de cara

📋

Uma condição caracterizada por níveis elevados de IgE no sangue, inflamação da pele e infecções respiratórias.

Pesquisas ativas
2 ensaios
14 total registrados no ClinicalTrials.gov
Publicações científicas
866 artigos
Último publicado: 2026
Medicamentos
4 registrados
ADALIMUMAB, SPESOLIMAB, DUPILUMAB

Tem tratamento?

4 medicamentos registrados
Ver detalhes, fases e interações →
ADALIMUMABSPESOLIMABDUPILUMABPIMECROLIMUS
🏥
SUS: Sem cobertura SUSScore: 0%
Você se identifica com essa condição?
O Raras está aqui pra te apoiar — com ou sem diagnóstico

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Entender a doença

Do básico ao detalhe, leia no seu ritmo

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Sinais e sintomas

O que aparece no corpo e com que frequência cada sintoma acontece

Partes do corpo afetadas

🧬
Pele e cabelo
38 sintomas
🫃
Digestivo
28 sintomas
🫁
Pulmão
16 sintomas
😀
Face
15 sintomas
🦴
Ossos e articulações
13 sintomas
🩸
Sangue
12 sintomas

+ 125 sintomas em outras categorias

Características mais comuns

Descamacão palmoplantar
Xantelasma
Erupção atrasada dos dentes
Fissura palatina
Atelectasia
Linfoma
301sintomas
Sem dados (301)

Os sintomas variam de pessoa para pessoa. Abaixo estão as 301 características clínicas mais associadas, ordenadas por frequência.

Descamacão palmoplantarPalmoplantar peeling
XantelasmaXanthelasma
Erupção atrasada dos dentesDelayed eruption of teeth
Fissura palatinaCleft palate
AtelectasiaAtelectasis

Linha do tempo da pesquisa

Publicações por ano — veja quando o interesse científico cresceu
Anos de pesquisa1desde 2026
Total histórico866PubMed
Últimos 10 anos200publicações
Pico202552 papers
Linha do tempo
2026Hoje · 2026🧪 1995Primeiro ensaio clínico📈 2025Ano de pico
Publicações por ano (últimos 10 anos)

Encontrou um erro ou informação desatualizada? Sugira uma correção →

Genética e causas

O que está alterado no DNA e como passa nas famílias

Genes associados

8 genes identificados com associação a esta condição.

ZNF341Zinc finger protein 341Disease-causing germline mutation(s) inTolerante
FUNÇÃO

Transcriptional activator of STAT3 involved in the regulation of immune homeostasis. Also able to activate STAT1 transcription

LOCALIZAÇÃO

Nucleus

MECANISMO DE DOENÇA

Hyper-IgE syndrome 3, autosomal recessive, with recurrent infections

An immunologic disorder characterized by skin bacterial infections in particular with Staphylococcus aureus, susceptibility to fungal infections such as chronic mucocutaneous candidiasis, atopic dermatitis, recurrent respiratory infections, bronchiectasis, and increased serum IgE and IgG. Immunologic work-up shows impaired differentiation of CD4+ T cells into T-helper 17 cells, decreased memory B cells, and often decreased NK cells. Some patients manifest extrahemapoietic features, including facial dysmorphism, abnormal dentition, alopecia, joint hypermobility and bone fractures. Disease onset is in early childhood.

EXPRESSÃO TECIDUAL(Ubíquo)
Cerebelo
9.9 TPM
Cérebro - Hemisfério cerebelar
9.5 TPM
Testículo
8.6 TPM
Baço
8.0 TPM
Próstata
7.8 TPM
OUTRAS DOENÇAS (1)
hyper-IgE recurrent infection syndrome 3, autosomal recessive
HGNC:15992UniProt:Q9BYN7
ERBINErbinCandidate gene tested inAltamente restrito
FUNÇÃO

Acts as an adapter for the receptor ERBB2, in epithelia. By binding the unphosphorylated 'Tyr-1248' of receptor ERBB2, it may contribute to stabilize this unphosphorylated state (PubMed:16203728). Inhibits NOD2-dependent NF-kappa-B signaling and pro-inflammatory cytokine secretion (PubMed:16203728)

LOCALIZAÇÃO

Cell junction, hemidesmosomeNucleus membraneBasolateral cell membrane

VIAS BIOLÓGICAS (10)
RAC3 GTPase cycleRHOG GTPase cycleRHOB GTPase cycleRAC1 GTPase cycleRAC2 GTPase cycle
EXPRESSÃO TECIDUAL(Ubíquo)
Fibroblastos
43.8 TPM
Brain Spinal cord cervical c-1
41.7 TPM
Nervo tibial
36.2 TPM
Linfócitos
34.0 TPM
Substância negra
31.9 TPM
OUTRAS DOENÇAS (1)
autosomal dominant combined immunodeficiency due to ERBIN deficiency
HGNC:15842UniProt:Q96RT1
IL6RInterleukin-6 receptor subunit alphaDisease-causing germline mutation(s) inTolerante
FUNÇÃO

Part of the receptor for interleukin 6. Binds to IL6 with low affinity, but does not transduce a signal (PubMed:28265003). Signal activation necessitate an association with IL6ST. Activation leads to the regulation of the immune response, acute-phase reactions and hematopoiesis (PubMed:30995492, PubMed:31235509). The interaction with membrane-bound IL6R and IL6ST stimulates 'classic signaling', the restricted expression of the IL6R limits classic IL6 signaling to only a few tissues such as the l

LOCALIZAÇÃO

Cell membraneSecreted

VIAS BIOLÓGICAS (6)
MAPK3 (ERK1) activationMAPK1 (ERK2) activationInterleukin-6 signalingPotential therapeutics for SARSTranscriptional regulation of granulopoiesis
MECANISMO DE DOENÇA

Hyper-IgE syndrome 5, autosomal recessive, with recurrent infections

An immunologic disorder characterized by recurrent sinopulmonary and deep skin infections, mostly caused by bacteria, including H.influenza and S.aureus. Additional features include asthma, atopic dermatitis, and impaired inflammatory responses during infection. Disease onset is in early infancy.

EXPRESSÃO TECIDUAL(Ubíquo)
Músculo esquelético
67.2 TPM
Sangue
52.7 TPM
Fígado
38.0 TPM
Pulmão
29.4 TPM
Esôfago - Muscular
27.0 TPM
OUTRAS DOENÇAS (2)
hyper-IgE recurrent infection syndrome 5, autosomal recessiveautosomal recessive combined immunodeficiency due to IL6R deficiency
HGNC:6019UniProt:P08887
DOCK8Dedicator of cytokinesis protein 8Disease-causing germline mutation(s) inTolerante
FUNÇÃO

Guanine nucleotide exchange factor (GEF) which specifically activates small GTPase CDC42 by exchanging bound GDP for free GTP (PubMed:22461490, PubMed:28028151). During immune responses, required for interstitial dendritic cell (DC) migration by locally activating CDC42 at the leading edge membrane of DC (By similarity). Required for CD4(+) T-cell migration in response to chemokine stimulation by promoting CDC42 activation at T cell leading edge membrane (PubMed:28028151). Is involved in NK cell

LOCALIZAÇÃO

CytoplasmCell membraneCell projection, lamellipodium membrane

VIAS BIOLÓGICAS (4)
Factors involved in megakaryocyte development and platelet productionRHOJ GTPase cycleRAC1 GTPase cycleCDC42 GTPase cycle
MECANISMO DE DOENÇA

Hyper-IgE syndrome 2, autosomal recessive, with recurrent infections

A rare disorder characterized by immunodeficiency, recurrent infections, eczema, increased serum IgE, eosinophilia and lack of connective tissue and skeletal involvement.

EXPRESSÃO TECIDUAL(Ubíquo)
Baço
49.4 TPM
Linfócitos
49.0 TPM
Sangue
26.3 TPM
Esôfago - Muscular
19.5 TPM
Pulmão
15.5 TPM
OUTRAS DOENÇAS (2)
combined immunodeficiency due to DOCK8 deficiencyautosomal dominant non-syndromic intellectual disability
HGNC:19191UniProt:Q8NF50
IL6STInterleukin-6 receptor subunit betaDisease-causing germline mutation(s) inAltamente restrito
FUNÇÃO

Signal-transducing molecule (PubMed:2261637). The receptor systems for IL6, LIF, OSM, CNTF, IL11, CTF1 and BSF3 can utilize IL6ST for initiating signal transmission. Binding of IL6 to IL6R induces IL6ST homodimerization and formation of a high-affinity receptor complex, which activates the intracellular JAK-MAPK and JAK-STAT3 signaling pathways (PubMed:19915009, PubMed:2261637, PubMed:23294003). That causes phosphorylation of IL6ST tyrosine residues which in turn activates STAT3 (PubMed:19915009

LOCALIZAÇÃO

Cell membraneSecreted

VIAS BIOLÓGICAS (4)
Interleukin-6 signalingInterleukin-27 signalingIL-6-type cytokine receptor ligand interactionsInterleukin-35 Signalling
MECANISMO DE DOENÇA

Hyper-IgE syndrome 4A, autosomal dominant, with recurrent infections

An immunologic disorder characterized by recurrent mainly sino-pulmonary infections associated with increased serum IgE. Some patients have onset of symptoms in early childhood and develop complications, including bronchiectasis or hemoptysis, whereas others have later onset of less severe infections. Immunologic workup usually shows normal leukocyte levels, although some patients may demonstrate alterations in lymphocyte subsets, including T cells. Affected individuals also have variable skeletal abnormalities, including high-arched palate, hyperextensible joints, scoliosis, and bone fractures.

EXPRESSÃO TECIDUAL(Ubíquo)
Fibroblastos
214.0 TPM
Adipose Visceral Omentum
117.2 TPM
Pulmão
116.9 TPM
Nervo tibial
116.5 TPM
Tecido adiposo
113.4 TPM
OUTRAS DOENÇAS (7)
Stuve-Wiedemann syndrome 2hyper-IgE recurrent infection syndrome 4A, autosomal dominanthyper-IgE recurrent infection syndrome 4, autosomal recessiveimmunodeficiency 94 with autoinflammation and dysmorphic facies
HGNC:6021UniProt:P40189
STAT6Signal transducer and activator of transcription 6Disease-causing germline mutation(s) inRestrito
FUNÇÃO

Carries out a dual function: signal transduction and activation of transcription. Involved in IL4/interleukin-4- and IL3/interleukin-3-mediated signaling

LOCALIZAÇÃO

CytoplasmNucleus

VIAS BIOLÓGICAS (3)
Interleukin-4 and Interleukin-13 signalingDownstream signal transductionSTAT6-mediated induction of chemokines
MECANISMO DE DOENÇA

Hyper-IgE syndrome 6, autosomal dominant, with recurrent infections

An immunologic disorder characterized by severe allergic disease with onset in infancy. Common features are treatment-resistant atopic dermatitis, food allergies, asthma, eosinophilic gastrointestinal disease, and severe episodes of anaphylaxis. Half of the patients present with recurrent skin, respiratory, and viral infections. Clinical laboratory testing is notable for eosinophilia and markedly elevated serum IgE levels.

EXPRESSÃO TECIDUAL(Ubíquo)
Ovário
219.3 TPM
Cervix Endocervix
215.3 TPM
Baço
213.2 TPM
Cervix Ectocervix
212.7 TPM
Útero
205.9 TPM
OUTRAS DOENÇAS (2)
hyper-IgE syndrome 6, autosomal dominant, with recurrent infectionssolitary fibrous tumor
HGNC:11368UniProt:P42226
STAT3Signal transducer and activator of transcription 3Disease-causing germline mutation(s) inAltamente restrito
FUNÇÃO

Signal transducer and transcription activator that mediates cellular responses to interleukins, KITLG/SCF, LEP and other growth factors (PubMed:10688651, PubMed:12359225, PubMed:12873986, PubMed:15194700, PubMed:15653507, PubMed:16285960, PubMed:17344214, PubMed:18242580, PubMed:18782771, PubMed:22306293, PubMed:23084476, PubMed:28262505, PubMed:32929201, PubMed:38404237). Once activated, recruits coactivators, such as NCOA1 or MED1, to the promoter region of the target gene (PubMed:15653507, Pu

LOCALIZAÇÃO

CytoplasmNucleus

VIAS BIOLÓGICAS (10)
Interleukin-20 family signalingDownstream signal transductionInterleukin-15 signalingSignaling by SCF-KITInterleukin-9 signaling
MECANISMO DE DOENÇA

Hyper-IgE syndrome 1, autosomal dominant, with recurrent infections

A rare disorder of immunity and connective tissue characterized by immunodeficiency, chronic eosinophilia, distinctive coarse facial appearance, abnormal dentition, hyperextensibility of the joints, and bone fractures.

EXPRESSÃO TECIDUAL(Ubíquo)
Pulmão
173.0 TPM
Artéria tibial
145.7 TPM
Aorta
144.8 TPM
Adipose Visceral Omentum
140.2 TPM
Fallopian Tube
136.9 TPM
OUTRAS DOENÇAS (7)
hyper-IgE recurrent infection syndrome 1, autosomal dominantSTAT3-related early-onset multisystem autoimmune diseasebreast implant-associated anaplastic large cell lymphomaacute promyelocytic leukemia
HGNC:11364UniProt:P40763
SPINK5Serine protease inhibitor Kazal-type 5Disease-causing germline mutation(s) inTolerante
FUNÇÃO

Serine protease inhibitor, probably important for the anti-inflammatory and/or antimicrobial protection of mucous epithelia. Contribute to the integrity and protective barrier function of the skin by regulating the activity of defense-activating and desquamation-involved proteases. Inhibits KLK5, its major target, in a pH-dependent manner. Inhibits KLK7, KLK14 CASP14, and trypsin

LOCALIZAÇÃO

Secreted

VIAS BIOLÓGICAS (1)
Differentiation of Keratinocytes in Interfollicular Epidermis in Mammalian Skin
MECANISMO DE DOENÇA

Netherton syndrome

An autosomal recessive congenital ichthyosis associated with hair shaft abnormalities and anomalies of the immune system. Typical features are ichthyosis linearis circumflexa, ichthyosiform erythroderma, trichorrhexis invaginata (bamboo hair), atopic dermatitis, and hayfever. High postnatal mortality is due to failure to thrive, infections and hypernatremic dehydration.

EXPRESSÃO TECIDUAL(Tecido-específico)
Esôfago - Mucosa
1154.5 TPM
Vagina
666.4 TPM
Skin Sun Exposed Lower leg
328.5 TPM
Skin Not Sun Exposed Suprapubic
312.4 TPM
Glândula salivar
10.8 TPM
OUTRAS DOENÇAS (1)
Netherton syndrome
HGNC:15464UniProt:Q9NQ38

Medicamentos e terapias

ADALIMUMABPhase 2

Mecanismo: TNF-alpha inhibitor

SPESOLIMABPhase 2

Mecanismo: IL36 receptor antagonist

DUPILUMABPhase 2

Mecanismo: Interleukin-4 receptor subunit alpha antagonist

PIMECROLIMUSPhase 1

Mecanismo: FK506-binding protein 1A inhibitor

Ver mais no OpenTargets

Variantes genéticas (ClinVar)

112 variantes patogênicas registradas no ClinVar.

🧬 ZNF341: NM_001282933.2(ZNF341):c.1024C>T (p.Arg342Ter) ()
🧬 ZNF341: NM_001282933.2(ZNF341):c.400del (p.Ile134fs) ()
🧬 ZNF341: NM_001282933.2(ZNF341):c.1350C>A (p.Cys450Ter) ()
🧬 ZNF341: NM_001282933.2(ZNF341):c.1253del (p.Gln418fs) ()
🧬 ZNF341: NM_001282933.2(ZNF341):c.720del (p.Met240fs) ()
Ver todas no ClinVar

Classificação de variantes (ClinVar)

Distribuição de 15 variantes classificadas pelo ClinVar.

11
4
Patogênica (73.3%)
VUS (26.7%)
VARIANTES MAIS SIGNIFICATIVAS
STAT6: NM_003153.5(STAT6):c.1114G>A (p.Glu372Lys) [Pathogenic]
STAT6: NM_003153.5(STAT6):c.1555G>C (p.Asp519His) [Pathogenic]
STAT6: NM_003153.5(STAT6):c.1144G>C (p.Glu382Gln) [Pathogenic]
STAT6: NM_003153.5(STAT6):c.1255G>C (p.Asp419His) [Likely pathogenic]
STAT6: NM_003153.5(STAT6):c.1255G>T (p.Asp419Tyr) [Pathogenic]

Vias biológicas (Reactome)

63 vias biológicas associadas aos genes desta condição.

Signaling by ERBB2 Downregulation of ERBB2 signaling RHOA GTPase cycle RHOB GTPase cycle RHOC GTPase cycle RAC1 GTPase cycle RAC2 GTPase cycle RHOG GTPase cycle RAC3 GTPase cycle Constitutive Signaling by Overexpressed ERBB2 Drug-mediated inhibition of ERBB2 signaling Signaling by ERBB2 KD Mutants Resistance of ERBB2 KD mutants to trastuzumab Resistance of ERBB2 KD mutants to sapitinib Resistance of ERBB2 KD mutants to tesevatinib Resistance of ERBB2 KD mutants to neratinib Resistance of ERBB2 KD mutants to osimertinib Resistance of ERBB2 KD mutants to afatinib Resistance of ERBB2 KD mutants to AEE788 Resistance of ERBB2 KD mutants to lapatinib Signaling by ERBB2 ECD mutants Signaling by ERBB2 TMD/JMD mutants Drug resistance in ERBB2 TMD/JMD mutants Interleukin-6 signaling MAPK3 (ERK1) activation MAPK1 (ERK2) activation Interleukin-4 and Interleukin-13 signaling Transcriptional regulation of granulopoiesis Potential therapeutics for SARS CDC42 GTPase cycle RHOJ GTPase cycle Factors involved in megakaryocyte development and platelet production IL-6-type cytokine receptor ligand interactions Interleukin-35 Signalling Interleukin-27 signaling Downstream signal transduction STAT6-mediated induction of chemokines BH3-only proteins associate with and inactivate anti-apoptotic BCL-2 members Interleukin-7 signaling Signaling by SCF-KIT Signaling by cytosolic FGFR1 fusion mutants Signalling to STAT3 Signaling by ALK Senescence-Associated Secretory Phenotype (SASP) Signaling by Leptin POU5F1 (OCT4), SOX2, NANOG activate genes related to proliferation Association of TriC/CCT with target proteins during biosynthesis Transcriptional regulation of pluripotent stem cells Interleukin-10 signaling PTK6 Activates STAT3 Interleukin-20 family signaling MET activates STAT3 Interleukin-15 signaling Interleukin-9 signaling Interleukin-37 signaling Interleukin-23 signaling Interleukin-21 signaling Signaling by phosphorylated juxtamembrane, extracellular and kinase domain KIT mutants Signaling by PDGFRA transmembrane, juxtamembrane and kinase domain mutants Signaling by PDGFRA extracellular domain mutants Signaling by CSF3 (G-CSF) Formation of the cornified envelope Differentiation of Keratinocytes in Interfollicular Epidermis in Mammalian Skin

Diagnóstico

Os sinais que médicos procuram e os exames que confirmam

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Tratamento e manejo

Remédios, cuidados de apoio e o que precisa acompanhar

Pipeline de tratamentos
Pipeline regulatório — de medicamentos já aprovados a drogas em pesquisa exploratória.
2Fase 26
1Fase 13
·Pré-clínico1
Medicamentos catalogadosEnsaios clínicos· 4 medicamentos · 6 ensaios
Carregando informações de tratamento...

Onde tratar no SUS

Hospitais de referência no Brasil e o protocolo oficial do SUS (PCDT)

🇧🇷 Atendimento SUS — Síndrome de hiper IgE

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Pesquisa ativa

Ensaios clínicos abertos e novidades científicas recentes

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Outros ensaios clínicos

14 ensaios clínicos encontrados, 2 ativos.

Distribuição por fase
Ver todos no ClinicalTrials.gov
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Publicações mais relevantes

Timeline de publicações
431 papers (10 anos)
#1

JAK-STAT signaling: molecular mechanism and targeted treatment in dento-maxillofacial abnormalities.

International journal of oral science2026 Mar 05

Dento-maxillofacial abnormalities are highly prevalent and arise as a result of a variety of etiological factors, presenting substantial challenges to treatment. The JAK-STAT signaling plays a pivotal role in dentofacial development, regulating endochondral ossification, intramembranous ossification, dental follicle formation, and enamel development. Mutations in the JAK-STAT signaling lead to syndromes associated with severe dento-maxillofacial abnormalities, including Growth Hormone Insensitivity Syndrome and Autosomal Dominant Hyper-IgE Syndrome. Corresponding mouse disease models have been developed to simulate the phenotypes observed in clinical patients and investigate their underlying mechanism. Meanwhile, several medications targeting JAK-STAT signaling, including baricitinib and imatinib, have been developed for clinical application, demonstrating significant effects in skeletal disorders such as osteoporosis and osteoarthritis, indicating promising effects in development and abnormalities of dento-maxillofacial. In this review, we aim to summarize the role of JAK-STAT signaling in the development and abnormalities of dento-maxillofacial bone, and the relevant molecules that may be utilized for clinical treatment, to shed new light on the precise treatment of dento-maxillofacial abnormalities.

#2

Non-syndromic hyper-IgE in children: A practical approach.

The World Allergy Organization journal2026 Mar

Hyper-IgE, generally defined as serum IgE levels exceeding 2000 IU/mL, presents a common yet complex diagnostic challenge in pediatric practice. While elevated serum IgE are frequently observed in atopic conditions such as food allergy or atopic eczema, or parasitic infections, they may also signal underlying monogenic immunological diseases, specifically inborn errors of immunity (IEI) categorized under hyper-IgE syndrome (HIES). Distinguishing between common atopic diseases and HIES is essential, especially in children with early-onset, severe, or treatment-resistant presentations. This review focuses on non-syndromic causes of hyper-IgE in children, aiming to provide a practical, structured framework for clinicians. A broad array of conditions, including allergic diseases, infections, inflammatory disorders, malignancies, drug reactions, and environmental exposures, can result in elevated IgE levels. Given this wide differential, a systematic approach that incorporates detailed clinical history, physical examination, and targeted investigations is critical to guide diagnostic reasoning. To aid clinical decision-making, the authors propose a stepwise diagnostic algorithm that prioritizes common causes while also alerting clinicians to red flags suggestive of IEI or other rare conditions. This approach facilitates timely referral for immunologic or genetic evaluation when appropriate and minimizes unnecessary testing. Increased awareness of the diverse etiologies of hyper-IgE can improve diagnostic accuracy, enhance early intervention, and reduce morbidity. Future research should aim to refine diagnostic strategies, validate clinical algorithms, and develop standardized guidelines. Moreover, long-term data regarding characterization and subsequent follow-up of children with an isolated increase in serum IgE levels is fundamental to understanding the clinical and immunological trajectories of these patients.

#3

Oncostatin M receptor deficiency as a novel candidate genetic cause of autosomal recessive hyper-IgE syndrome.

Journal of human immunity2026 May 04

Hyper-IgE syndrome (HIES) is characterized by elevated serum IgE levels, eczema, and recurrent skin and pulmonary infections, classically caused by autosomal dominant (AD) STAT3 loss-of-function variants. Here we describe a patient presenting with elevated IgE levels, atopic eczema, chronic pulmonary aspergillosis, and bone fractures, homozygous for a rare missense variant in the oncostatin M receptor (OSMR) gene. We demonstrate that the patient OSMR V436D variant is deleterious and leads to decreased OSMR surface expression and impaired OSM-induced STAT3 phosphorylation. Blood profiling showed elevated IgE-expressing plasmablasts and peripheral T follicular helper cells and atypical memory B cells. A germinal center model revealed a B cell-extrinsic defect in concordance with a largely fibroblast-confined phenotype. Finally, reconstitution of patient fibroblasts led to functional complementation of the cellular phenotype. We propose OSMR deficiency as a novel genetic etiology of AR-HIES, resembling the clinical and immunological phenotype of STAT3 AD-HIES, but mediating its phenotypic profile mainly in the stromal rather than hematopoietic compartment.

#4

Orbital Abscess in an Infant With STAT3 Hyper-IgE Syndrome.

Ophthalmic plastic and reconstructive surgery2026 Mar 02

Orbital cellulitis (OC) is a rare diagnosis in infants, with limited numbers of cases reported in the literature to date. We report a 34‑day‑old female who presented with severe left-sided periorbital swelling and proptosis. Imaging confirmed a large orbital abscess with associated ethmoid sinusitis, and she underwent urgent exploration and drainage and initiation of broad‑spectrum intravenous antibiotics. Cultures grew methicillin‑sensitive Staphylococcus aureus. Postoperatively, she developed leukocytosis, eosinophilia, and recurrent skin abscesses, prompting immunologic evaluation. Genetic testing identified a novel STAT3 mutation in the SH2 domain consistent with Hyper‑IgE syndrome. This case highlights both the importance of prompt surgical and medical intervention in infantile orbital cellulitis and the need to consider underlying immune dysregulation when atypical clinical or laboratory findings are present. To our knowledge, this is the first reported case of infantile orbital cellulitis associated with Hyper-IgE syndrome, and the first report of this specific STAT3 variant causing hyper‑IgE syndrome.

#5

Neutrophil hyperresponsiveness contributes to lung pathology in STAT3V463Δ mice.

Journal of immunology (Baltimore, Md. : 1950)2026 Feb 09

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 expressing the STAT3V463Δ mutation, a common disease-associated variant. Following intratracheal infection with Pseudomonas aeruginosa, STAT3V463Δ mice exhibited pronounced alveolar damage, increased vascular congestion, and extensive leukocyte infiltration compared to wild-type (WT) controls. These changes were accompanied by elevated bacterial burden and significantly increased levels of pro-inflammatory cytokines and chemokines in the lung. Neutrophil recruitment to the lungs was markedly elevated, and surface expression of degranulation markers was enhanced in STAT3V463Δ neutrophils in vivo. To determine whether neutrophil hyperactivation was driven by intrinsic defects independent of microbial load, mice were challenged intratracheally with purified lipopolysaccharide (LPS), revealing similarly enhanced neutrophil degranulation and NETosis in STAT3V463Δ mice despite controlled PAMP exposure. Mechanistically, bone marrow-derived neutrophils (BMDNs) from STAT3V463Δ mice displayed heightened degranulation and NETosis in response to PMA or f-MLF stimulation. Together, these findings demonstrate that STAT3V463Δ drives neutrophil hyperresponsiveness, contributing to dysregulated inflammation and pulmonary tissue damage in AD-HIES.

Publicações recentes

Ver todas no PubMed

📚 EuropePMC463 artigos no totalmostrando 197

2026

Non-syndromic hyper-IgE in children: A practical approach.

The World Allergy Organization journal
2026

Oncostatin M receptor deficiency as a novel candidate genetic cause of autosomal recessive hyper-IgE syndrome.

Journal of human immunity
2026

JAK-STAT signaling: molecular mechanism and targeted treatment in dento-maxillofacial abnormalities.

International journal of oral science
2026

Orbital Abscess in an Infant With STAT3 Hyper-IgE Syndrome.

Ophthalmic plastic and reconstructive surgery
2026

Neutrophil hyperresponsiveness contributes to lung pathology in STAT3V463Δ mice.

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

Autosomal Dominant Hyper-IgE Syndrome Patients Retain IL10-Producing preTh17-Cells That Are Activated by Opportunistic Pathogens and Support IgE Production.

Allergy
2026

Clinical Spectrum of Cutaneous, Ocular, and Hair Manifestations in Patients With Inborn Errors of Immunity: Insights From a Single Center in Turkey.

Immunity, inflammation and disease
2026

STAT3-Mutated Hyper-IgE Syndrome With Retroperitoneal Abscess in Adolescence.

Clinical case reports
2026

SPINK5 Variants Drive Clinical Variability in Netherton Syndrome Through Th2/Th17 Skewing and Influence Therapeutic Outcomes.

The journal of allergy and clinical immunology. In practice
2026

DOCK8 and STAT3 cooperate to restrain IgE-inducing T follicular helper cells.

The Journal of experimental medicine
2026

Decreased IL-17-producing TH cells as a diagnostic marker for STAT signaling-related primary immunodeficiencies.

The journal of allergy and clinical immunology. Global
2025

An integrated platform for concurrent structural and single-nucleotide variants improves copy-number detection and reveals pathogenic alleles in undiagnosed Mendelian families.

Genome medicine
2025

STAT3 c.1915C > T variant-associated Hyper-IgE syndrome in a child: a case report.

Frontiers in pediatrics
2025

Recurrent Disseminated Talaromycosis Mimicking Liver Disease in a STAT3-Mutated HIES Patient: A Case Report.

Infection and drug resistance
2026

Recurrent severe infections in a child with STAT3-associated hyper-IgE syndrome.

JAAD case reports
2025

Efficacy of omalizumab in the treatment of STAT3 loss-of-function mutations associated with autosomal dominant hyperimmunoglobulin E syndrome-a case report.

Translational pediatrics
2026

Job's not done: BCG-itis as the first manifestation of hyper-IgE syndrome. A case report and review of the literature.

Clinical immunology (Orlando, Fla.)
2025

Progressive multifocal leukoencephalopathy in a young adult with DOCK8 deficiency: a case of JC virus reactivation in primary immunodeficiency.

Journal of neurovirology
2026

Successful Use of Tralokinumab in a Pediatric Patient With STAT3 Hyper-IgE Syndrome Following Dupilumab-Associated Conjunctivitis.

International journal of dermatology
2025

Understanding and Managing Hyper IgE Syndromes.

ImmunoTargets and therapy
2025

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

Molecular biomedicine
2026

Obesity and hepatic steatosis in STAT3 hyper-IgE syndrome.

The journal of allergy and clinical immunology. In practice
2025

Audiovestibular Dysfunction in Hyper-IgE Syndrome: A Systematic Review of Characteristics, Pathophysiology, Diagnosis, and Management.

International journal of molecular sciences
2025

Metagenomic next-generation sequencing: a game-changer in the diagnosis of unique intraocular infections.

Eye (London, England)
2025

A Novel Hypomorphic STAT3 Gene Variant in a 7-year-old Male with Hyper-IgE Syndrome.

Journal of clinical immunology
2025

Case Report: Dual molecular diagnosis of gain-of-function STAT1 mutation and regulatory STAT3 variant in a patient with a hyper-IgE-like phenotype.

Frontiers in immunology
2025

Pulmonary manifestations in Hyper-IgE syndrome.

Respiratory medicine
2026

Pediatric Severe Eosinophilia: Etiological Spectrum, Diagnostic Algorithm, and Case-Based Insights From a Tertiary Care Center.

International journal of laboratory hematology
2025

Immunogenetic investigation of WAS patients revealing impaired IL-6/STAT3 signaling in T cells.

Frontiers in immunology
2025

The prevalence of allergic manifestations in inborn errors of immunity: a retrospective cohort study.

BMC immunology
2025

Hyper IgE Syndrome: Imaging Clues to Diagnosis.

Indian journal of pediatrics
2025

Case report: anti-IL-6 autoantibodies in a patient with immune dysregulation, polyendocrinopathy, enteropathy, X-linked syndrome.

Frontiers in immunology
2025

A multicenter evaluation of the Filariasis IgG4 Rapid Test for detection of lymphatic filariasis.

Acta tropica
2025

Loss of Stat3 in Prx1+ Progenitors Impairs Molar Root Development.

Advanced biology
2025

Eosinophilic Pustular Folliculitis in a Child With Hyper-IgE Syndrome: A Case Report Emphasizing the Importance of Immunodeficiency Screening in Infancy.

The Journal of dermatology
2025

Extensive Cellulitic Infection and Tissue Necrosis in a Patient With Hyper IgE Syndrome: Surgical Management of a Rare Immunodeficiency.

Cureus
2025

Early Postmenopausal Fragility Fractures and Elevated IgE: Two Cases Suggesting Hyper-IgE Syndrome and a Novel Adverse Reaction to Romosozumab.

Calcified tissue international
2025

STAT3 haploinsufficiency is associated with autosomal dominant hyper-IgE syndrome.

Science advances
2025

Mouse Model of STAT3 Mutation Resulting in Job's Syndrome Diverges from Human Pathology.

International journal of molecular sciences
2025

Signal Transducer and Activator of Transcription 3 (STAT3) Variant p.K709N Causes Hyper-IgE Syndrome Likely by Impaired STAT3-Dimer Formation.

European journal of immunology
2026

Co-Existence of IL6ST and MEFV Pathogenic Variant in a Patient With Hyper-IgE Syndrome.

Immunology
2025

Infection prevention in patients with inborn errors of immunity: Insights from Japan's nationwide study.

Pediatrics international : official journal of the Japan Pediatric Society
2025

Upadacitinib for Treatment of Hyper-IgE Syndrome.

JAMA dermatology
2025

Persistent Neutropenia and Atopy in an Adolescent: A Subtle Presentation of Phosphoglucomutase 3 Deficiency.

Cureus
2025

Hyper-IgE syndrome: A rare case report.

The journal of allergy and clinical immunology. Global
2025

Hyperimmunoglobulin syndromes: A review of HIGM, HIES, and HIDS.

Journal of translational autoimmunity
2025

Back With Vengeance: Delayed Gastrointestinal Sequelae of Histoplasmosis in a Patient With STAT3 Hyper-IgE Syndrome.

ACG case reports journal
2025

A case of ichthyosis prematurity syndrome mimicking hyper-IgE syndrome.

Annals of allergy, asthma & immunology : official publication of the American College of Allergy, Asthma, & Immunology
2025

Global Burden of Allergies: Mechanisms of Development, Challenges in Diagnosis, and Treatment.

Life (Basel, Switzerland)
2025

Allogeneic hematopoietic stem cell transplantation for STAT3 hyper-IgE syndrome: a worldwide study.

Blood advances
2025

Fine mapping of heterozygous IL6ST nonsense variants underlying autosomal dominant hyper-IgE syndrome.

JCI insight
2025

Case Report: Biliary hemorrhage by intrahepatic pseudoaneurysm and asymptomatic right coronary artery pseudoaneurysm in a patient with STAT3 hyper IgE syndrome.

Frontiers in immunology
2025

Empyema Necessitatis and Hyper IgE Syndrome: An Unusual Association.

Open respiratory archives
2025

Pulmonary features and stage of disease in adult patients with hyper-IgE syndrome: a single-centre clinical study and literature review.

Orphanet journal of rare diseases
2025

Haploidentical stem cell transplantation in DOCK8 deficiency: a case report of successful outcomes.

Blood coagulation & fibrinolysis : an international journal in haemostasis and thrombosis
2025

Omalizumab: a broader role in dermatology? Evidence and the road ahead.

Italian journal of dermatology and venereology
2025

Dermatologic presentations of hyper IgE syndrome in pediatric patients.

Allergy, asthma, and clinical immunology : official journal of the Canadian Society of Allergy and Clinical Immunology
2025

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

American journal of respiratory and critical care medicine
2025

Dominant-Negative Versus Gain-of-Function STAT3 Defects: A Systematic Review on Epidemiological, Clinical, Immunological, and Molecular Aspects.

The journal of allergy and clinical immunology. In practice
2025

Severe Atopic Dermatitis: Clinical Confusion With Hyper IgE Syndrome.

Cureus
2025

Hyper-IgE Syndrome: A Case Report with Insights from Bioinformatics Analysis of Key Pathways and Genes.

Infection and drug resistance
2025

Hyper IgE Syndrome: Bridging the Gap Between Immunodeficiency, Atopy, and Allergic Diseases.

Current allergy and asthma reports
2025

Coexistence of T-Cell Lymphoblastic Lymphoma and Ichthyosis Vulgaris: A Case Report.

Case reports in oncological medicine
2025

Pulmonary Aspergillosis and Low HIES Score in a Family with STAT3 N-Terminal Domain Mutation.

Journal of clinical immunology
2025

Human inborn errors of immunity underlying Talaromyces marneffei infections: a multicenter, retrospective cohort study.

Frontiers in immunology
2025

Break through the mold: Hyper-IgE syndrome as a vehicle for invasive aspergillosis.

Respiratory medicine case reports
2024

Relation between dysbiosis and inborn errors of immunity.

World journal of methodology
2024

Clinical and molecular profile of 20 patients with DOCK8 deficiency-a single-center experience from Southern India.

Immunologic research
2024

DOCK8 gene mutation alters cell subsets, BCR signaling, and cell metabolism in B cells.

Cell death & disease
2024

Pulmonary manifestations in hyper IgE syndrome: A case series and review of Indian literature.

Lung India : official organ of Indian Chest Society
2024

Pathophysiology of Congenital High Production of IgE and Its Consequences: A Narrative Review Uncovering a Neglected Setting of Disorders.

Life (Basel, Switzerland)
2024

Phenotypes of 126 Moroccan HIES patients according to NIH Score.

La Tunisie medicale
2024

DOCK8 deficiency due to a deep intronic variant in two kindreds with hyper-IgE syndrome.

Clinical immunology (Orlando, Fla.)
2024

Low incidence of primary immunodeficiency-associated cancers in children at a tertiary care pediatric hospital in Pakistan: a blessing in disguise or wet behind the ears?

Ecancermedicalscience
2025

Improvement in Atopic Dermatitis and Recurrent Infection With Dupilumab in Children With Distinct Genetic Types of Hyper-IgE Syndrome: A Case Series and Literature Review.

Pediatric dermatology
2024

Rapid identification of primary atopic disorders (PAD) by a clinical landmark-guided, upfront use of genomic sequencing.

Allergologie select
2024

Syk protein inhibitors treatment for the allergic symptoms associated with hyper immunoglobulin E syndromes: A focused on a computational approach.

International journal of immunopathology and pharmacology
2024

Challenges in diagnosing and managing hyper-IgE syndrome in a resource-limited setting: a case report.

Annals of medicine and surgery (2012)
2024

Unraveling the unphosphorylated STAT3-unphosphorylated NF-κB pathway in loss of function STAT3 Hyper IgE syndrome.

Frontiers in immunology
2024

Dysregulated Airway Host Defense in Hyper IgE Syndrome due to STAT3 Mutations.

bioRxiv : the preprint server for biology
2024

Comprehensive Multidisciplinary Management of Hyper-IgE Syndrome in an 11-Year-Old Female: A Pediatric Case Report.

Cureus
2024

Immunoglobulin class-switch recombination: Mechanism, regulation, and related diseases.

MedComm
2024

Neutrophil-avid nanocarrier uptake by STAT3 dominant-negative hyper-IgE syndrome patient neutrophils.

Life science alliance
2024

Identifying potentially undiagnosed individuals with hyper-IgE syndrome using a scoring system.

Annals of allergy, asthma & immunology : official publication of the American College of Allergy, Asthma, & Immunology
2024

Obstructive uropathy in STAT 3 hyper immunoglobulin E syndrome: A 5 year old Middle Eastern boy.

Saudi medical journal
2024

Flow cytometry-based diagnostic approach for inborn errors of immunity: experience from Algeria.

Frontiers in immunology
2024

Exploring the Link Between Profuse Warts and Hyper-Immunoglobulin E (IgE) Syndrome: A Pediatric Case Report.

Cureus
2024

Autosomal Recessive Hyper-IgE Syndrome in a Child With Beta Thalassemia Trait: A Case Report.

Cureus
2024

A term infant with severe hypereosinophilia secondary to CMV infection and the STAT1 gene mutation: a case report : List of authors.

BMC pediatrics
2024

Staphylococcus aureus Serine protease-like protein A (SplA) induces IL-8 by keratinocytes and synergizes with IL-17A.

Cytokine
2024

Viral infections and inborn errors of immunity.

Current opinion in infectious diseases
2024

Extracellular Vesicles based STAT3 delivery as innovative therapeutic approach to restore STAT3 signaling deficiency.

New biotechnology
2024

Resolving persistent air leaks associated with autosomal dominant hyper-IgE syndrome using one-way endobronchial valves: report of cases.

AME case reports
2024

An Indian Family with Autosomal Dominant Hyper-IgE Syndrome Due to IL6ST Defect.

Journal of clinical immunology
2024

The treatment efficacy of dupilumab in autosomal dominant hyper-immunoglobulin E syndrome with severe atopic dermatitis.

Asia Pacific allergy
2024

Differential Diagnosis and Interdisciplinary Workup of a Pediatric Patient With an Unknown Immune Condition: Chronic Respiratory Distress Secondary to Viral Illness and Developmental Consequences.

Cureus
2024

Clinical, immunological, and genetic description of a Mexican cohort of patients with DOCK8 deficiency.

Pediatric allergy and immunology : official publication of the European Society of Pediatric Allergy and Immunology
2024

Hyper-IgE syndrome: a case report.

Annals of medicine and surgery (2012)
2024

Hyper-IgE syndrome in an 11 year old female presenting with acneiform rash.

Skin health and disease
2023

Genetic Susceptibility to Fungal Infections.

Advanced biomedical research
2023

The Human GP130 Cytokine Receptor and Its Expression-an Atlas and Functional Taxonomy of Genetic Variants.

Journal of clinical immunology
2025

Omalizumab and dupilumab for the treatment of autosomal-recessive DOCK8 hyper-IgE syndrome.

Indian journal of dermatology, venereology and leprology
2024

STAT3 Deficiency Alters the Macrophage Activation Pattern and Enhances Matrix Metalloproteinase 9 Expression during Staphylococcal Pneumonia.

Journal of immunology (Baltimore, Md. : 1950)
2024

Primary immunodeficiency diseases of adults: a review of pulmonary complication imaging findings.

European radiology
2023

A systematic review regarding the prevalence of malignancy in patients with the hyper-IgE syndrome.

Clinical and experimental medicine
2023

Intraoral and maxillofacial abnormalities in patients with autosomal dominant hyper-IgE syndrome.

Central-European journal of immunology
2023

Hyper IgE Syndrome With Multiple Respiratory Infections. Review About a Clinical Case.

Open respiratory archives
2023

Interventional pulmonary procedures and their outcomes in patients with STAT3 hyper IgE syndrome.

BMC surgery
2023

Hyper IgE syndrome-related disease treated with dupilumab: A case report.

Clinical case reports
2023

Efficacy of Dupilumab in Treating Atopic Dermatitis With Recurrent Eczema Herpeticum in a Patient With DOCK8-Deficiency Hyper-IgE Syndrome: A Case Report.

Cureus
2024

Expanding the clinical and immunological phenotype of prolidase deficiency: A case report.

Pediatric dermatology
2023

Single-cell multi-omics sequencing reveals the immunological disturbance underlying STAT3-V637M Hyper-IgE syndrome.

International immunopharmacology
2023

Kawasaki Disease and Inborn Errors of Immunity: Exploring the Link and Implications.

Diagnostics (Basel, Switzerland)
2023

The pulmonary effects of STAT3 deficiency.

The Journal of allergy and clinical immunology
2023

Atypical Cutaneous Viral Infections Reveal an Inborn Error of Immunity in 8 Patients.

Microorganisms
2023

Successful Use of Fosmanogepix for Treatment of Rare Highly Resistant Cutaneous Fusariosis in a Pediatric Patient With STAT3 Hyper-Immunoglobulin E Syndrome and End-Stage Kidney Disease.

Open forum infectious diseases
2023

New Dominant-Negative IL6ST Variants Expand the Immunological and Clinical Spectrum of GP130-Dependent Hyper-IgE Syndrome.

Journal of clinical immunology
2023

Intrapleural therapy for pleural infection from bronchopleural fistula in an adult with hyper-IgE syndrome.

Respirology case reports
2023

Quality of Life Evaluation in Saudi Arabian Pediatric Patients with Primary Immunodeficiency Diseases Receiving 20% Subcutaneous IgG Infusions at Home.

Journal of clinical immunology
2023

Successful treatment of DOCK8 deficiency by allogeneic hematopoietic cell transplantation from alternative donors.

International journal of hematology
2023

In Silico Analyses of All STAT3 Missense Variants Leading to Explore Divergent AD-HIES Clinical Phenotypes.

Evolutionary bioinformatics online
2023

Microbiome and Its Dysbiosis in Inborn Errors of Immunity.

Pathogens (Basel, Switzerland)
2023

Hyper-IgE syndrome presenting with early life craniosynostosis in monozygotic twin sisters.

Pediatric allergy and immunology : official publication of the European Society of Pediatric Allergy and Immunology
2023

Loss of Stat3 in Osterix+ cells impairs dental hard tissues development.

Cell & bioscience
2023

Disseminated Talaromyces marneffei Infection With STAT3-Hyper-IgE Syndrome: A Case Series and Literature Review.

Open forum infectious diseases
2023

Hematopoietic stem cell Transplantation in Children with very Early Onset Inflammatory Bowel Disease Secondary to Monogenic Disorders of immune-dysregulation.

Indian journal of hematology & blood transfusion : an official journal of Indian Society of Hematology and Blood Transfusion
2022

A Young Woman with Autosomal Dominant Hyper Immunoglobulin E (job's) Syndrome Presenting with Acute Abdomen: a Case Report.

Medical archives (Sarajevo, Bosnia and Herzegovina)
2022

[Combined immunodeficiency due to DOCK8 deficiency. State of the art].

Revista alergia Mexico (Tecamachalco, Puebla, Mexico : 1993)
2023

Germline Mosaicism in STAT3: A Pitfall for Genetic Diagnosis, Counseling, and Therapy of Hyper-IgE Syndrome.

Dermatitis : contact, atopic, occupational, drug
2023

Lupus Nephritis in an Adolescent Girl With Hyper-Immunoglobulin E.

Cureus
2023

Idiopathic non-cirrhotic portal hypertension in a patient with Talaromyces marneffei infection: a case report.

BMC infectious diseases
2023

Food Allergy Characteristics Associated With Coexisting Eosinophilic Esophagitis in FARE Registry Participants.

The journal of allergy and clinical immunology. In practice
2023

Multi-Omics Profiling in PGM3 and STAT3 Deficiencies: A Tale of Two Patients.

International journal of molecular sciences
2023

Dupilumab zur Behandlung von Genodermatosen: Eine systematische Übersicht.

Journal der Deutschen Dermatologischen Gesellschaft = Journal of the German Society of Dermatology : JDDG
2023

Dupilumab in the treatment of genodermatosis: A systematic review.

Journal der Deutschen Dermatologischen Gesellschaft = Journal of the German Society of Dermatology : JDDG
2023

STAT3 mutation-associated airway epithelial defects in Job syndrome.

The Journal of allergy and clinical immunology
2023

Autoimmune myositis and autoimmune hemolytic anemia in two sisters with DOCK8-deficient hyper-IgE syndrome.

Immunologic research
2022

Dominant-negative signal transducer and activator of transcription (STAT)3 variants in adult patients: A single center experience.

Frontiers in immunology
2023

STAT6 gain-of-function variant exacerbates multiple allergic symptoms.

The Journal of allergy and clinical immunology
2023

Primary Invasive Cutaneous Fusariosis in Patients with STAT3 Hyper-IgE Syndrome.

Journal of clinical immunology
2023

The signal transducer and activator of transcription 3 at the center of the causative gene network of the hyper-IgE syndrome.

Current opinion in immunology
2022

Antibody deficiencies with normal IgG in adults with Non-cystic fibrosis bronchiectasis or recurrent pneumonia: Cross-sectional study.

Colombia medica (Cali, Colombia)
2022

Allele-Specific Disruption of a Common STAT3 Autosomal Dominant Allele Is Not Sufficient to Restore Downstream Signaling in Patient-Derived T Cells.

Genes
2023

A challenging differential diagnosis in a patient with autosomal dominant STAT3 deficiency.

Pediatric pulmonology
2022

Eosinophilic gastrointestinal disorders in patients with inborn errors of immunity: Data from the USIDNET registry.

Frontiers in immunology
2022

Inborn errors of immunity and related microbiome.

Frontiers in immunology
2022

Treosulfan-based Reduced-intensity Allogeneic Hematopoietic Cell Transplantation in Adults With Primary Immunodeficiency: A Case Series.

Anticancer research
2023

Disseminated BCG Disease in a Patient with Hyper IgE Syndrome due to Dominant-Negative STAT3 Mutation-Case Report.

Journal of clinical immunology
2022

Immunoglobulin Disorders and the Oral Cavity: A Narrative Review.

Journal of clinical medicine
2022

A progressing inflammatory pulmonary infiltrate in a patient with hyper IgE syndrome.

SAGE open medical case reports
2022

Main human inborn errors of immunity leading to fungal infections.

Clinical microbiology and infection : the official publication of the European Society of Clinical Microbiology and Infectious Diseases
2022

Beyond Infections: New Warning Signs for Inborn Errors of Immunity in Children.

Frontiers in pediatrics
2022

STAT3-confusion-of-function: Beyond the loss and gain dualism.

The Journal of allergy and clinical immunology
2022

Clearance of atypical cutaneous manifestations of hyper-IgE syndrome with dupilumab.

Pediatric dermatology
2022

Utility of targeted next generation sequencing for inborn errors of immunity at a tertiary care centre in North India.

Scientific reports
2022

[Hyper-IgE syndrome in adults characterized by disseminated mixed infection: a case report and literature review].

Zhonghua jie he he hu xi za zhi = Zhonghua jiehe he huxi zazhi = Chinese journal of tuberculosis and respiratory diseases
2022

Molecular Assessment of Staphylococcus Aureus Strains in STAT3 Hyper-IgE Syndrome Patients.

Journal of clinical immunology
2022

Hyper-IgE and Carcinoma in CADINS Disease.

Frontiers in immunology
2022

Inborn errors of immunity underlying a susceptibility to pyogenic infections: from innate immune system deficiency to complex phenotypes.

Clinical microbiology and infection : the official publication of the European Society of Clinical Microbiology and Infectious Diseases
2022

Omalizumab for STAT3 Hyper-IgE Syndromes in Adulthood: A Case Report and Literature Review.

Frontiers in medicine
2022

An unusual cause of facial wound in a child: Hyper IgE syndrome-associated Noma neonatorum.

International wound journal
2022

Remission of eczema and recovery of Th1 polarization following treatment with Dupilumab in STAT3 hyper IgE syndrome.

Pediatric allergy and immunology : official publication of the European Society of Pediatric Allergy and Immunology
2022

Hyper-IgE syndrome caused by DOCK8 mutation with a tumour-like lesion of the lip: a case report.

International journal of oral and maxillofacial surgery
2021

Proteomics Profiling to Distinguish DOCK8 Deficiency From Atopic Dermatitis.

Frontiers in allergy
2022

CRISPR/Cas-Based Gene Editing Strategies for DOCK8 Immunodeficiency Syndrome.

Frontiers in genome editing
2022

Bronchial inflammation biomarker patterns link humoral immunodeficiency with bronchiectasis-related small airway dysfunction.

Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology
2022

A 36-year-old pregnant woman with hyperimmunoglobulinemia E.

Ginekologia polska
2022

Successful Management of Mixed Mycosis in HIV-Negative Patients With Different Immune Status: A Case Series Report.

Frontiers in cellular and infection microbiology
2022

Recurrent Breast Abscesses in a Female with Autosomal Dominant Hyper-IgE Syndrome.

Journal of clinical immunology
2022

Hyper IgE Syndrome in an Isolated Population in Israel.

Frontiers in immunology
2022

Malignancy in STAT3 Deficient Hyper IgE Syndrome.

Journal of clinical immunology
2024

Recurrent Skin Ulcers with Facial Dysmorphism and Sinopulmonary Infections: Thinking Beyond Hyper-IgE Syndrome.

Journal of pediatric genetics
2022

Chronic pulmonary aspergillosis in a patient with hyper-IgE syndrome.

Respirology case reports
2021

Essential Role of STAT3 Signaling in Hair Follicle Homeostasis.

Frontiers in immunology
2022

Management of Peripheral T-Cell Lymphoma in Children and Adolescents Including STAT 3 Mutation Hyper-IgE Syndrome: One Size Does Not Fit All.

Journal of pediatric hematology/oncology
2022

Patient with atopic dermatitis, hyper IgE syndrome and ulcerative colitis, treated successfully with dupilumab during pregnancy.

Dermatologic therapy
2021

Defective Toll-Like Receptors Driven B Cell Response in Hyper IgE Syndrome Patients With STAT3 Mutations.

Frontiers in pediatrics
2022

The Immune Deficiency and Dysregulation Activity (IDDA2.1 'Kaleidoscope') Score and Other Clinical Measures in Inborn Errors of Immunity.

Journal of clinical immunology
2021

Inborn errors of immunity: Recent progress.

The Journal of allergy and clinical immunology
2021

Case Report: Dupilumab Successfully Controls Severe Eczema in a Child With Elevated IgE Levels and Recurrent Skin Infections.

Frontiers in pediatrics
2021

A Prospective Survey of Skin Manifestations in Children With Inborn Errors of Immunity From a National Registry Over 17 Years.

Frontiers in immunology
2022

Hyper-IgE Syndrome due to an Elusive Novel Intronic Homozygous Variant in DOCK8.

Journal of clinical immunology
2022

Profound differences in IgE and IgG recognition of micro-arrayed allergens in hyper-IgE syndromes.

Allergy
2021

Very Elevated IgE, Atopy, and Severe Infection: A Genomics-Based Diagnostic Approach to a Spectrum of Diseases.

Case reports in immunology
2022

Novel mutations of TYK2 leading to divergent clinical phenotypes.

Pediatric allergy and immunology : official publication of the European Society of Pediatric Allergy and Immunology
2022

Relieving job: Dupilumab in autosomal dominant STAT3 hyper-IgE syndrome.

The journal of allergy and clinical immunology. In practice
2021

Rare clinical presentations of hyper-IgE syndrome in a patient with dental abnormalities: A case report.

Clinical case reports
2021

One Gene, Many Facets: Multiple Immune Pathway Dysregulation in SOCS1 Haploinsufficiency.

Frontiers in immunology
2021

Hyper-IgE syndrome, 2021 update.

Allergology international : official journal of the Japanese Society of Allergology
2021

Investigating the Variation of TREC/KREC in Combined Immunodeficiencies.

Iranian journal of allergy, asthma, and immunology
2021

Dupilumab for STAT3-Hyper-IgE Syndrome With Refractory Intestinal Complication.

Pediatrics
2021

Genetic Analysis of a Cohort of 275 Patients with Hyper-IgE Syndromes and/or Chronic Mucocutaneous Candidiasis.

Journal of clinical immunology
2021

[Hyper IgE syndrome: atopic dermatitis as first manifestation. Case report].

Archivos argentinos de pediatria
2021

Autosomal recessive hyper-IgE syndrome caused by DOCK8 gene mutation with new clinical features: a case report.

BMC neurology
2021

Treatment of severe atopic dermatitis and eosinophilic esophagitis with dupilumab in a 14-year-old boy with autosomal dominant hyper-IgE syndrome.

The journal of allergy and clinical immunology. In practice
2022

One-year intravenous immunoglobulin replacement therapy: efficacy in reducing hospital admissions in pediatric patients with Inborn Errors of Immunity.

Jornal de pediatria
2021

Case Report: Interleukin-2 Receptor Common Gamma Chain Defect Presented as a Hyper-IgE Syndrome.

Frontiers in immunology
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Referências e fontes

Bases de dados externas citadas neste artigo

Publicações científicas

Artigos indexados no PubMed ligados a esta doença no grafo RarasNet — título, periódico e PMID direto da fonte, sem intermediação de IA.

  1. JAK-STAT signaling: molecular mechanism and targeted treatment in dento-maxillofacial abnormalities.
    International journal of oral science· 2026· PMID 41781377mais citado
  2. Non-syndromic hyper-IgE in children: A practical approach.
    The World Allergy Organization journal· 2026· PMID 41798765mais citado
  3. Oncostatin M receptor deficiency as a novel candidate genetic cause of autosomal recessive hyper-IgE syndrome.
    Journal of human immunity· 2026· PMID 41783139mais citado
  4. Orbital Abscess in an Infant With STAT3 Hyper-IgE Syndrome.
    Ophthalmic plastic and reconstructive surgery· 2026· PMID 41771060mais citado
  5. Neutrophil hyperresponsiveness contributes to lung pathology in STAT3V463Δ mice.
    Journal of immunology (Baltimore, Md. : 1950)· 2026· PMID 41764721mais citado
  6. STAT3 isoform dynamics reveal robust splice ratio maintenance across cytokine-activated human immune cells.
    Front Immunol· 2026· PMID 41993160recente
  7. STAT3 dominant negative Hyper-IgE syndrome: A patient report with actionable genomic findings.
    Eur J Med Genet· 2026· PMID 41985740recente
  8. Dock8 regulates Th2 cell differentiation through ANXA1.
    Fundam Res· 2026· PMID 41971794recente
  9. An Infant With Hyper IgE Syndrome Mimicking Acute Leukemia.
    Clin Case Rep· 2026· PMID 41938639recente
  10. A Novel Phosphoglucomutase-3 Gene Variant Causing Milder Phenotype in Two Families.
    J Clin Immunol· 2026· PMID 41904308recente

Bases de dados e fontes oficiais

Identificadores e referências canônicas usadas para montar este verbete.

  1. ORPHA:331223(Orphanet)
  2. MONDO:0018037(MONDO)
  3. GARD:10956(GARD (NIH))
  4. Variantes catalogadas(ClinVar)
  5. Busca completa no PubMed(PubMed)
  6. Q55787700(Wikidata)

Dados compilados pelo RarasNet a partir de fontes abertas (Orphanet, OMIM, MONDO, PubMed/EuropePMC, ClinicalTrials.gov, DATASUS, PCDT/MS). Este conteúdo é informativo e não substitui avaliação médica.

Conteúdo mantido por Agente Raras · Médicos e pesquisadores podem colaborar

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