Trial reportThe Journal of clinical investigation2018
TNF overproduction impairs epithelial staphylococcal response in hyper IgE syndrome.
Trial report in The Journal of clinical investigation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
28 citing papers in PubMed, 30 citations in OpenAlex.
- Differential responses to folic acid in an established keloid fibroblast cell line are mediated by JAK1/2 and STAT3.PloS one · 2021Trial
- Therapeutic responses toScience translational medicine · 2020Trial
- Impaired angiogenesis and extracellular matrix metabolism in autosomal-dominant hyper-IgE syndrome.The Journal of clinical investigation · 2020Trial
- Discovery of Natural Compound α-Hederin via Large-Scale Screening as a Targeted JAK/STAT3 Inhibitor for Ovarian Cancer Therapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Topical Steroid Withdrawal Is a Targetable Excess of Mitochondrial NAD.The Journal of investigative dermatology · 2025Article
- Skin imaging mass spectrometry of controls versus atopic dermatitis patients with and withoutiScience · 2025Article
- Inborn errors of immunity with susceptibility toFrontiers in pediatrics · 2024Review
- Shotgun metagenomic sequencing on skin microbiome indicates dysbiosis exists prior to the onset of atopic dermatitis.Allergy · 2023Article
- Deficiencies and Dysregulation of STAT Pathways That Drive Inborn Errors of Immunity: Lessons from Patients and Mouse Models of Disease.Journal of immunology (Baltimore, Md. : 1950) · 2023Review
- Article
- Molecular Assessment of Staphylococcus Aureus Strains in STAT3 Hyper-IgE Syndrome Patients.Journal of clinical immunology · 2022Article
- STAT3 is critical for skeletal development and bone homeostasis by regulating osteogenesis.Nature communications · 2021Article
- Infections in the monogenic autoimmune syndrome APECED.Current opinion in immunology · 2021Review
- Response to Comments on "Aberrant type 1 immunity drives susceptibility to mucosal fungal infections".Science (New York, N.Y.) · 2021Article
- Assessing the effects of common topical exposures on skin bacteria associated with atopic dermatitis.Skin health and disease · 2021Article
- Delayed diagnosis of hyperimmunoglobulin E syndrome with STAT3 mutation in mainland China: a case report and literature review.The Journal of international medical research · 2021Review
- Aberrant type 1 immunity drives susceptibility to mucosal fungal infections.Science (New York, N.Y.) · 2021Article
- Therapeutic candidates for keloid scars identified by qualitative review of scratch assay research for wound healing.PloS one · 2021Review
- A Novel STAT3 Mutation in a Patient with Hyper-IgE Syndrome Diagnosed with a Severe Necrotizing Pulmonary Infection.Journal of asthma and allergy · 2021Article
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
21 authors at 5 institutions in 3 countries.
Funding
Abstract
Autosomal dominant hyper IgE syndrome (AD-HIES), or Job's syndrome, is a primary immune deficiency caused by dominant-negative mutations in STAT3. Recurrent Staphylococcus aureus skin abscesses are a defining feature of this syndrome. A widely held hypothesis that defects in peripheral Th17 differentiation confer this susceptibility has never been directly evaluated. To assess the cutaneous immune response in AD-HIES, we induced suction blisters in healthy volunteers (HVs) and patients with AD-HIES and then challenged the wound with lethally irradiated bacteria. We show that cutaneous production of IL-17A and IL-17F was normal in patients with AD-HIES. Overproduction of TNF-α differentiated the responses in AD-HIES from HVs. This was associated with reduced IL-10 family signaling in blister-infiltrating cells and defective epithelial cell function. Mouse models of AD-HIES recapitulated these aberrant epithelial responses to S. aureus and involved defective epithelial-to-mesenchymal transition (EMT) rather than a failure of bacterial killing. Defective responses in mouse models of AD-HIES and primary keratinocyte cultures from patients with AD-HIES could be reversed by TNF-α blockade and by drugs with reported modulatory effects on EMT. Our results identify these as potential therapeutic approaches in patients with AD-HIES suffering S. aureus infections.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.