Evidence map›Paper›PMID 31712904›Full record

ReviewCurrent rheumatology reports2019

The Pathogenesis of Ankylosing Spondylitis: an Update.

Susanne Juhl Pedersen, Walter P Maksymowych

Abstract readReview
PubMed Publisher
In one paragraph

Review in Current rheumatology reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed, 3 pooled it
7.5field-weighted citation impact, top 2% 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

66 citing papers in PubMed, 3 syntheses or guidelines pooled it, 115 citations in OpenAlex.

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  10. Interleukin 15 and autoimmune disorders: pathophysiology, therapeutic potential, and clinical implications.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
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6 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

2 authors at 2 institutions in 2 countries.

Susanne Juhl PedersenCopenhagen Center for Arthritis Research (COPECARE), Center for Rheumatology and Spine Disease, Rigshospitalet, Valdemar Hansens Vej 17, 2600, Glostrup, Denmark. susanne_juhl_ped@dadlnet.dk.ORCID 0000-0002-6500-9263
Walter P MaksymowychDepartment of Medicine, University of Alberta, Edmonton, Alberta, T6G 2S2, Canada.ORCID 0000-0002-1291-1755
Glostrup Hospital · DKUniversity of Alberta · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purpose of reviewAnkylosing spondyloarthritis (AS) is a chronic inflammatory disease that involves the axial joints and entheses. Extra-spinal manifestations such as anterior uveitis, psoriasis, and colitis also occur frequently. This review on the pathogenesis of AS includes an update on the recent discoveries within the field. RECENT

findingsHLA-B*27 is still considered of major importance in the pathogenesis, and it has recently been shown to profoundly affect the gut microbiome and its metabolites and the handling of bacteria during infection. Biochemical and biophysical properties of HLA-B*27 influence its ability to misfold, to induce an endoplasmic reticulum stress response, and to promote autophagy/unfolded protein responses (UPR). HLA-B*27 free heavy chains may induce inflammation through T cells, NK cells, and myeloid cells. Induction of UPR genes results in release of tumor necrosis factor-α (TNF-α), interleukin-17 (IL-17), IL-23, and interferon-γ and increase in T helper (Th) 17 cells. Several other HLA-B and non-B molecules have been associated with AS, although their role in the pathogenesis is unknown. Genotypes of endoplasmic reticulum aminopeptidases (ERAP) 1 and 2 have been associated with alterations in the antigenic pool expressed by HLA-B*27 molecules. In the gut, innate immune cells type 3 (ILC3) influence T cell expression of IL-17 and IL-22. Gamma-delta (γ/δ) T cells are induced by IL-23 to produce IL-17. IL-7 induces mucosa-associated invariant T (MAIT) cells to produce IL-17. Besides the microbiome, zonulin may be important through its effects on the permeability of tight junctions in the intestinal epithelial barrier.

Indexed as

Unfolded Protein ResponseGastrointestinal MicrobiomeHLA-B27 AntigenHumansInflammationSpondylitis, AnkylosingHLA-B27 AntigenAnkylosing spondylitisGenesHLA-B*27ImmunologyMicrobiomePathogenesis

Identifiers

PMID31712904
OpenAlexW2984945126

What OpenQuestion 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 OpenQuestion graph.