Mouse models of type I interferonopathies.

Abstract readReview

In one paragraph

Review in Human molecular genetics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it

0cells of the map it votes in

0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors.

Domnica LucaInstitute of Cardiovascular Immunology, University Hospital Bonn, University of Bonn, Venusberg-Campus 1, Bonn 53127, Germany.

Hiroki KatoInstitute of Cardiovascular Immunology, University Hospital Bonn, University of Bonn, Venusberg-Campus 1, Bonn 53127, Germany.ORCID 0000-0002-9571-4895

Funding

Deutsche Forschungsgemeinschaft 369799452Deutsche Forschungsgemeinschaft EXC2151-390873048Deutsche Forschungsgemeinschaft TRR237

6 · The paper itself

Abstract

Type I interferonopathies are severe monogenic diseases caused by mutations that result in chronically upregulated production of type I interferon. They present with a broad variety of symptoms, the mechanisms of which are being extensively studied. Mouse models of type I interferonopathies are an important resource for this purpose, and in this context, we review several key molecular and phenotypic findings that are advancing our understanding of the respective diseases. We focus on genotypes related to nucleic acid metabolism, sensing by cytosolic receptors and downstream signalling.

Indexed as

Disease Models, AnimalInterferon Type IAnimalsHumansMiceMutationSignal TransductionInterferon Type IAutoimmunityInnate immunityInnate sensorsType I interferon

Identifiers

PMID39680957

DOI10.1093/hmg/ddae187

PMCPMC12501977

What OpenQuestion holds

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Registered trials

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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.