ReviewCurrent opinion in immunology2023
Inherited human ZNF341 deficiency.
Review in Current opinion in immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
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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
13 citing papers in PubMed, 15 citations in OpenAlex.
- Single-cell analysis identifies a VIM+ glioma stem-like vascular-immune state linked to myeloid OSM signaling and CEBPD activity.Frontiers in immunology · 2026Article
- Atopic dermatitis in inborn errors of immunity: at the interface of immunodeficiency and immune dysregulation.Immunologic research · 2025Review
- 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 · 2025Review
- Hyper IgE Syndromes: Understanding, Management, and Future Perspectives: A Narrative Review.Health science reports · 2025Article
- Reproducible processing of TCGA regulatory networks.GigaScience · 2025Article
- Inborn Errors of Immunity Presenting with Early-Onset Severe Atopy.Medicina (Kaunas, Lithuania) · 2025Review
- Cytokine signaling defects in primary atopic diseases-an updated review.Frontiers in allergy · 2025Review
- Understanding and Managing Hyper IgE Syndromes.ImmunoTargets and therapy · 2025Review
- The genetics of hyper IgE syndromes.Frontiers in immunology · 2025Review
- Pathophysiology of Congenital High Production of IgE and Its Consequences: A Narrative Review Uncovering a Neglected Setting of Disorders.Life (Basel, Switzerland) · 2024Review
- Article
- Transcription factor defects in inborn errors of immunity with atopy.Frontiers in allergy · 2023Review
- 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 dermatologyReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 3 countries.
Funding
Abstract
Typical hyper-IgE syndromes (HIES) are caused by autosomal-dominant-negative (DN) variants of STAT3 (Signal Transducer And Activator Of Transcription 3) or IL6ST (Interleukin 6 Cytokine Family Signal Transducer), biallelic partial loss-of-function (LOF) variants of IL6ST, or biallelic complete LOF variants of ZNF341 (Zinc Finger Protein 341). Including the two new cases described in this review, only 20 patients with autosomal-recessive (AR) ZNF341 deficiency have ever been reported. Patients with AR ZNF341 deficiency have clinical and immunological phenotypes resembling those of patients with autosomal-dominant STAT3 deficiency, but with a usually milder clinical presentation and lower NK (Natural Killer) cell counts. ZNF341-deficient cells have 50% the normal level of STAT3 in the resting state. However, as there is no clear evidence that STAT3 haploinsufficiency causes HIES, this decrease alone is probably insufficient to explain the HIES phenotype observed in the ZNF341-deficient patients. The combination of decreased basal expression level and impaired autoinduction of STAT3 observed in ZNF341-deficient lymphocytes is considered a more likely pathophysiological mechanism. We review here what is currently known about the ZNF341 gene and ZNF341 deficiency, and briefly discuss possible roles for this protein in addition to its control of STAT3 activity.
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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.