Evidence map›Paper›PMID 35911727›Full record

ArticleFrontiers in immunology2022

A Novel Type I Interferon Primed Dendritic Cell Subpopulation in TREX1 Mutant Chilblain Lupus Patients.

Anne Eugster, Denise Müller, Anne Gompf, Susanne Reinhardt, Annett Lindner, Michelle Ashton, Nick Zimmermann, Stefan Beissert, Ezio Bonifacio, Claudia Günther

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.7field-weighted citation impact, top 33% of its field
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

6 citing papers in PubMed, 9 citations in OpenAlex.

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    Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 3 institutions in 1 country.

Anne EugsterCenter for Regenerative Therapies Dresden, Faculty of Medicine Technische Universität (TU), Dresden, Germany.
Denise MüllerCenter for Regenerative Therapies Dresden, Faculty of Medicine Technische Universität (TU), Dresden, Germany.
Anne GompfCenter for Regenerative Therapies Dresden, Faculty of Medicine Technische Universität (TU), Dresden, Germany.
Susanne ReinhardtCenter for Molecular and Cellular Bioengineering (CMCB), DRESDEN-Concept Genome Center Technische Universität, Dresden, Germany.
Annett LindnerCenter for Regenerative Therapies Dresden, Faculty of Medicine Technische Universität (TU), Dresden, Germany.
Michelle AshtonCenter for Regenerative Therapies Dresden, Faculty of Medicine Technische Universität (TU), Dresden, Germany.
Nick ZimmermannFaculty of Medicine, Paul Langerhans Institute Dresden of Helmholtz Centre Munich at University Clinic Carl Gustav Carus of Technische Univeristät (TU) Dresden, Dresden, Germany.
Stefan BeissertFaculty of Medicine, Paul Langerhans Institute Dresden of Helmholtz Centre Munich at University Clinic Carl Gustav Carus of Technische Univeristät (TU) Dresden, Dresden, Germany.
Ezio BonifacioCenter for Regenerative Therapies Dresden, Faculty of Medicine Technische Universität (TU), Dresden, Germany.
Claudia GüntherFaculty of Medicine, Paul Langerhans Institute Dresden of Helmholtz Centre Munich at University Clinic Carl Gustav Carus of Technische Univeristät (TU) Dresden, Dresden, Germany.
Technische Universität Dresden · DEUniversity Hospital Carl Gustav Carus · DEPaul Langerhans Institute Dresden · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Heterozygous TREX1 mutations are associated with monogenic familial chilblain lupus and represent a risk factor for developing systemic lupus erythematosus. These interferonopathies originate from chronic type I interferon stimulation due to sensing of inadequately accumulating nucleic acids. We here analysed the composition of dendritic cell (DC) subsets, central stimulators of immune responses, in patients with TREX1 deficiency. We performed single-cell RNA-sequencing of peripheral blood DCs and monocytes from two patients with familial chilblain lupus and heterozygous mutations in TREX1 and from controls. Type I interferon pathway genes were strongly upregulated in patients. Cell frequencies of the myeloid and plasmacytoid DC and of monocyte populations in patients and controls were similar, but we describe a novel DC subpopulation highly enriched in patients: a myeloid DC CD1C

Indexed as

Dendritic CellsLupus Erythematosus, CutaneousLupus Erythematosus, DiscoidChilblainsExodeoxyribonucleasesHumansInterferon Type IPhosphoproteinsExodeoxyribonucleasesInterferon Type IPhosphoproteinsthree prime repair exonuclease 1dendritic Cells (DC)Lamin A/CLMNAmonogenic familial chilblain lupusSLETrex1Type I interferons

Identifiers

PMID35911727
PMCPMC9327789
OpenAlexW4285085650

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.