Evidence map›Paper›PMID 34113018›Full record

ReviewNature reviews. Rheumatology2021

Ankylosing spondylitis: an autoimmune or autoinflammatory disease?

Daniele Mauro, Ranjeny Thomas, Giuliana Guggino, Rik Lories, Matthew A Brown, Francesco Ciccia

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Rheumatology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 207 papers, 6 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
207citing papers in PubMed, 6 pooled it
42.0field-weighted citation impact, top 1% 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

207 citing papers in PubMed, 6 syntheses or guidelines pooled it, 338 citations in OpenAlex.

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  15. From copper imbalance to immunometabolic remodeling: cuproptosis-related vulnerability and therapeutic hypotheses in autoimmune diseases.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Review
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147 more citing papers are in PubMed but not listed here.

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 5 institutions in 4 countries.

Daniele MauroDipartimento di Medicina di Precisione, Università della Campania L. Vanvitelli, Naples, Italy.
Ranjeny ThomasThe University of Queensland Diamantina Institute, The University of Queensland, Woolloongabba, Queensland, Australia.ORCID 0000-0002-0518-8386
Giuliana GugginoDipartimento PROMISE, Section of Rheumatology, University of Palermo, Palermo, Italy.
Rik LoriesSkeletal Biology and Engineering Research Center, KU Leuven, Leuven, Belgium.
Matthew A BrownGuy's and St Thomas' NHS Foundation Trust and King's College London NIHR Biomedical Research Centre, London, UK.ORCID 0000-0003-0538-8211
Francesco CicciaDipartimento di Medicina di Precisione, Università della Campania L. Vanvitelli, Naples, Italy. francesco.ciccia@unicampania.it.ORCID 0000-0002-9352-1264
University of Campania "Luigi Vanvitelli" · ITKing's College London · GBKU Leuven · BEThe University of Queensland · AUUniversity of Palermo · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ankylosing spondylitis (AS) is a chronic inflammatory disorder of unknown aetiology. Unlike other systemic autoimmune diseases, in AS, the innate immune system has a dominant role characterized by aberrant activity of innate and innate-like immune cells, including γδ T cells, group 3 innate lymphoid cells, neutrophils, mucosal-associated invariant T cells and mast cells, at sites predisposed to the disease. The intestine is involved in disease manifestations, as it is at the forefront of the interaction between the mucosal-associated immune cells and the intestinal microbiota. Similarly, biomechanical factors, such as entheseal micro-trauma, might also be involved in the pathogenesis of the articular manifestation of AS, and sentinel immune cells located in the entheses could provide links between local damage, genetic predisposition and the development of chronic inflammation. Although these elements might support the autoinflammatory nature of AS, studies demonstrating the presence of autoantibodies (such as anti-CD74, anti-sclerostin and anti-noggin antibodies) and evidence of activation and clonal expansion of T cell populations support an autoimmune component to the disease. This Review presents the evidence for autoinflammation and the evidence for autoimmunity in AS and, by discussing the pathophysiological factors associated with each, aims to reconcile the two hypotheses.

Indexed as

AnimalsAutoimmune DiseasesHereditary Autoinflammatory DiseasesHumansSpondylitis, Ankylosing

Identifiers

PMID34113018
OpenAlexW3169346015

What Socratic 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 Socratic graph.