Evidence map›Paper›PMID 39063175›Full record

ArticleInternational journal of molecular sciences2024

Toll-like Receptor Homologue CD180 Ligation of B Cells Upregulates Type I IFN Signature in Diffuse Cutaneous Systemic Sclerosis.

Szabina Erdő-Bonyár, Judit Rapp, Rovéna Subicz, Kristóf Filipánits, Tünde Minier, Gábor Kumánovics, László Czirják, Tímea Berki, Diána Simon

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in International journal of molecular sciences, 2024. 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. Article
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

9 authors.

Szabina Erdő-BonyárDepartment of Immunology and Biotechnology, Clinical Center, Medical School, University of Pécs, H-7624 Pécs, Hungary.ORCID 0000-0002-9597-8487
Judit RappDepartment of Immunology and Biotechnology, Clinical Center, Medical School, University of Pécs, H-7624 Pécs, Hungary.
Rovéna SubiczDepartment of Immunology and Biotechnology, Clinical Center, Medical School, University of Pécs, H-7624 Pécs, Hungary.
Kristóf FilipánitsDepartment of Rheumatology and Immunology, Clinical Center, Medical School, University of Pécs, H-7632 Pécs, Hungary.
Tünde MinierDepartment of Rheumatology and Immunology, Clinical Center, Medical School, University of Pécs, H-7632 Pécs, Hungary.ORCID 0000-0003-0983-2092
Gábor KumánovicsDepartment of Rheumatology and Immunology, Clinical Center, Medical School, University of Pécs, H-7632 Pécs, Hungary.ORCID 0000-0001-8500-2918
László CzirjákDepartment of Rheumatology and Immunology, Clinical Center, Medical School, University of Pécs, H-7632 Pécs, Hungary.
Tímea BerkiDepartment of Immunology and Biotechnology, Clinical Center, Medical School, University of Pécs, H-7624 Pécs, Hungary.
Diána SimonDepartment of Immunology and Biotechnology, Clinical Center, Medical School, University of Pécs, H-7624 Pécs, Hungary.

Funding

Hungarian National Research, Development and Innovation Fund OTKA FK-139028New National Excellence Program of the Ministry for Innovation and Technology from the Source of the National Research, Development and Innovation Fund ÚNKP-23-5Thematic Excellence Program 2021 Health Sub-programme of the Ministry for Innovation and Technology in Hungary, within the framework of the EGA-10 project of the Pécs of University TKP-2021-EGA-10
6 · The paper itself

Abstract

Type I interferon (IFN-I) signaling has been shown to be upregulated in systemic sclerosis (SSc). Dysregulated B-cell functions, including antigen presentation, as well as antibody and cytokine production, all of which may be affected by IFN-I signaling, play an important role in the pathogenesis of the disease. We investigated the IFN-I signature in 71 patients with the more severe form of the disease, diffuse cutaneous SSc (dcSSc), and 33 healthy controls (HCs). Activation via Toll-like receptors (TLRs) can influence the IFN-I signaling cascade; thus, we analyzed the effects of the TLR homologue CD180 ligation on the IFN-I signature in B cells. CD180 stimulation augmented the phosphorylation of signal transducer and activator of transcription 1 (STAT1) in dcSSc B cells (

Indexed as

Antigens, CDAutoantibodiesB-LymphocytesInterferon Type IAdultAgedFemaleHumansMaleMiddle AgedReceptor, Interferon alpha-betaScleroderma, DiffuseSignal TransductionSTAT1 Transcription FactorUp-RegulationAntigens, CDAutoantibodiesCD180 protein, humanInterferon Type IReceptor, Interferon alpha-betaSTAT1 protein, humanSTAT1 Transcription Factoranti-IFN-α autoantibodiesanti-IFN-ω autoantibodiesB cellsCD180IFN-I receptorinterferon (IFN)signal transducer and activator of transcription 1systemic sclerosisToll-like receptor

Identifiers

PMID39063175
PMCPMC11277506

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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.