Evidence map›Paper›PMID 35837382›Full record

ReviewFrontiers in immunology2022

Can Antinuclear Antibodies Have a Pathogenic Role in Systemic Sclerosis?

Aurélien Chepy, Louisa Bourel, Vincent Koether, David Launay, Sylvain Dubucquoi, Vincent Sobanski

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 1 pooled it
5.7field-weighted citation impact, top 3% 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

18 citing papers in PubMed, 1 synthesis or guideline pooled it, 41 citations in OpenAlex.

  1. Pooled it
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  7. Article
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  14. Biomarkers in Systemic Sclerosis: An Overview.Current issues in molecular biology · 2023
    Review
  15. Article
  16. Review
  17. Article
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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

6 authors at 3 institutions in 1 country.

Aurélien ChepyUniv. Lille, Inserm, CHU Lille, U1286-INFINITE-Institute for Translational Research in Inflammation, Lille, France.
Louisa BourelUniv. Lille, Inserm, CHU Lille, U1286-INFINITE-Institute for Translational Research in Inflammation, Lille, France.
Vincent KoetherUniv. Lille, Inserm, CHU Lille, U1286-INFINITE-Institute for Translational Research in Inflammation, Lille, France.
David LaunayUniv. Lille, Inserm, CHU Lille, U1286-INFINITE-Institute for Translational Research in Inflammation, Lille, France.
Sylvain DubucquoiUniv. Lille, Inserm, CHU Lille, U1286-INFINITE-Institute for Translational Research in Inflammation, Lille, France.
Vincent SobanskiUniv. Lille, Inserm, CHU Lille, U1286-INFINITE-Institute for Translational Research in Inflammation, Lille, France.
Institute for Translational Research in InflammationLille Inflammation Research International Center · FRCentre Hospitalier Universitaire de Lille · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Systemic sclerosis (SSc) is a connective tissue disease characterized by extensive fibrosis of the skin and internal organs, associated with vasculopathy and autoimmune features. Antinuclear antibodies (ANA) are found in almost all SSc patients and constitute strong diagnosis and prognosis biomarkers. However, it remains unclear whether ANA are simple bystanders or if they can have a role in the pathophysiology of the disease. One might think that the nuclear nature of their targets prevents any accessibility to autoantibodies. Nevertheless, recent data suggest that ANA could be pathogenic or at least contribute to the perennation of the disease. We review here first the indirect clues of the contribution of ANA to SSc: they are associated to the disease subtypes, they may precede disease onset, their titer correlates with disease activity and severity, there is an association between molecular subsets, and some patients can respond to B-cell targeting therapy. Then, we describe in a second part the mechanisms of ANA production in SSc from individual genetic background to post-transcriptional modifications of neoantigens. Finally, we elaborate on the potential mechanisms of pathogenicity: ANA could be pathogenic through immune-complex-mediated mechanisms; other processes potentially involve molecular mimicry and ANA penetration into the target cell, with a focus on anti-topoisomerase-I antibodies, which are the most probable candidate to play a role in the pathophysiology of SSc. Finally, we outline some technical and conceptual ways to improve our understanding in this field.

Indexed as

Antibodies, AntinuclearScleroderma, SystemicAutoantibodiesFibrosisHumansAntibodies, AntinuclearAutoantibodiesantibodiesantinuclear antibodies (ANA)biomarkerspathogenic antibodysystemic sclerosis

Identifiers

PMID35837382
PMCPMC9274282
OpenAlexW4283661583

What OpenQuestion holds

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LicenceCC BY
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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.