Evidence map›Paper›PMID 41783139›Full record

ArticleJournal of human immunity2026

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

Sisse Andersen, Kristian Assing, Julie Jensen, Line Dahlerup Rasmussen, Christian B Laursen, Christoffer D Dellgren, Daniëla Maria Hinke, Søren E Degn, Trine H Mogensen

Abstract read
In one paragraph

Article in Journal of human immunity, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

  1. Article
  2. Human germline biallelic loss-of-functionJournal of human immunity · 2026
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors.

Sisse Andersen *Department of Biomedicine, Aarhus University, Aarhus, Denmark.ORCID https://orcid.org/0009-0006-6090-1996
Kristian Assing *Department of Clinical Immunology, Odense University Hospital, Odense, Denmark.ORCID https://orcid.org/0000-0001-8744-1615
Julie JensenDepartment of Biomedicine, Aarhus University, Aarhus, Denmark.ORCID https://orcid.org/0009-0002-9704-5442
Line Dahlerup RasmussenDepartment of Infectious Diseases, Odense University Hospital, Odense, Denmark.ORCID https://orcid.org/0000-0003-0853-0893
Christian B LaursenDepartment of Pulmonology, Odense University Hospital, Odense, Denmark.ORCID https://orcid.org/0000-0001-6382-9906
Christoffer D DellgrenDepartment of Clinical genetics, Odense University Hospital, Odense, Denmark.ORCID https://orcid.org/0000-0003-4841-5187
Daniëla Maria HinkeDepartment of Biomedicine, Aarhus University, Aarhus, Denmark.ORCID https://orcid.org/0000-0002-3932-8762
Søren E DegnDepartment of Biomedicine, Aarhus University, Aarhus, Denmark.ORCID https://orcid.org/0000-0001-5409-045X
Trine H MogensenDepartment of Biomedicine, Aarhus University, Aarhus, Denmark.ORCID https://orcid.org/0000-0002-1853-9704

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

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 (

Identifiers

PMID41783139
PMCPMC12955778

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.