ArticleCurrent allergy and asthma reports2008
Genetic origins of hyper-IgE syndrome.
Article in Current allergy and asthma reports, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 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
11 citing papers in PubMed, 33 citations in OpenAlex.
- A progressing inflammatory pulmonary infiltrate in a patient with hyper IgE syndrome.SAGE open medical case reports · 2022Article
- Review
- Updates on T helper type 17 immunity in respiratory disease.Immunology · 2019Review
- Clinical Manifestations and Genetic Analysis of 17 Patients with Autosomal Dominant Hyper-IgE Syndrome in Mainland China: New Reports and a Literature Review.Journal of clinical immunology · 2017Review
- Antibody blockade of IL-17 family cytokines in immunity to acute murine oral mucosal candidiasis.Journal of leukocyte biology · 2016Article
- Hyper Ig E syndrome (Job syndrome, HIES) - radiological images of pulmonary complications on the basis of three cases.Polish journal of radiology · 2012Article
- The hyperimmunoglobulin E syndrome--clinical manifestation diversity in primary immune deficiency.Orphanet journal of rare diseases · 2011Review
- Recent advances in the IL-17 cytokine family.Current opinion in immunology · 2011Review
- Regulation and dysregulation of immunoglobulin E: a molecular and clinical perspective.Clinical and molecular allergy : CMA · 2010Article
- Human defensins and LL-37 in mucosal immunity.Journal of leukocyte biology · 2010Review
- Molecular explanation for the contradiction between systemic Th17 defect and localized bacterial infection in hyper-IgE syndrome.The Journal of experimental medicine · 2009Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hyper-IgE syndrome (HIES) is a complex primary immunodeficiency characterized by high serum IgE, chronic eczematoid dermatitis, and recurrent extracellular bacterial infections. Two types of HIES have been reported: type 1 and type 2. Type 1 HIES displays abnormalities in multiple systems, including the skeletal, dental, and immune systems, whereas type 2 shows abnormalities confined to the immune system. We recently identified hypomorphic mutations in the signal transducer and activator of transcription 3 (STAT3) gene in type 1 HIES and a null mutation in the tyrosine kinase 2 (Tyk2) gene, accompanied by susceptibility to intracellular bacteria in type 2 HIES. Analyses of cytokine responses in both types of HIES revealed that severe defects in the signal transduction for multiple cytokines, including interleukin-6 and interleukin-23, are leading to impaired T-helper type 17 function. These findings suggest that HIES is caused by the defects in multiple cytokine signals and that the susceptibility to various infections in HIES is associated with the T-helper type 17 defect.
Indexed as
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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.