Evidence map›Paper›PMID 33893896›Full record

ReviewCurrent rheumatology reports2021

Recent Updates in the Immunopathology of Type 3 Immunity-Mediated Enthesitis.

Akihiro Nakamura, Nigil Haroon

Abstract readReview
PubMed Publisher
In one paragraph

Review in Current rheumatology reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

9 citing papers in PubMed, 16 citations in OpenAlex.

  1. Review
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  9. Interleukin-17A (IL-17A): A silent amplifier of COVID-19.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2021
    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

2 authors at 1 institution in 1 country.

Akihiro NakamuraSchroeder Arthritis Institute, University Health Network, Toronto, Ontario, Canada.ORCID 0000-0002-4258-1603
Nigil HaroonSchroeder Arthritis Institute, University Health Network, Toronto, Ontario, Canada. Nigil.Haroon@uhn.ca.ORCID 0000-0003-3210-4771
University Health Network · CA

Funding

CIHR
6 · The paper itself

Abstract

purpose of reviewEnthesitis is a cardinal feature of spondyloarthritis (SpA). Despite increasing available treatments, challenges remain in adequately controlling inflammation and subsequent new bone formation (NBF) in entheses; thus, a better understanding of the immunopathogenesis is warranted. RECENT

findingsIncreasing evidence has identified immune cells playing key roles in enthesitis such as γδ T cells and group 3 innate lymphoid cells (ILC3), possibly with site-specific regulatory systems. The presence of T cells producing interleukin (IL)-17 independent of IL-23 in human spinal entheses was recently reported, which may corroborate the discrepancy between recent clinical trials and pre-clinical studies. In addition, the contribution of myeloid cells has also been focused in both human and pre-clinical SpA models. Moreover, not only the IL-23/IL-17 signaling, but other key type 3 immunity mediators, such as IL-22 and granulocyte-macrophage colony-stimulating factor (GM-CSF), have been reported as pivotal cytokines in inflammation and NBF of entheses. Immune cells demonstrating distinct features orchestrate entheses, leading to the complex landscape of enthesitis. However, recent advances in understanding the immunopathogenesis may provide new therapeutic targets and future research directions.

Indexed as

EnthesopathySpondylarthritisHumansImmunity, InnateInterleukin-17Interleukin-23LymphocytesInterleukin-17Interleukin-23EnthesitisGM-CSFIL-22IL23/IL-17 axisSpondyloarthritis

Identifiers

PMID33893896
OpenAlexW3156335055

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.