Evidence map›Paper›PMID 28270233›Full record

ReviewArthritis research & therapy2017

Mechanistic rationales for targeting interleukin-17A in spondyloarthritis.

Siba P Raychaudhuri, Smriti K Raychaudhuri

Open access · goldAbstract readReview
In one paragraph

Review in Arthritis research & therapy, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
3.2field-weighted citation impact, top 7% 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

33 citing papers in PubMed, 71 citations in OpenAlex.

  1. Trial
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  7. JAK/STAT as a Potential Therapeutic Target for Osteolytic Diseases.International journal of molecular sciences · 2023
    Review
  8. Article
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  15. Phenotype and pathological significance of MCAMMolecular biology reports · 2021
    Article
  16. Article
  17. Review
  18. Article
  19. Frontiers in immunology · 2021
    Article
  20. Review
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.

Siba P RaychaudhuriVA Medical Center Sacramento, Division of Rheumatology & Immunology, Sacramento, CA, USA. sraychaudhuri@ucdavis.edu.
Smriti K RaychaudhuriVA Medical Center Sacramento, Division of Rheumatology & Immunology, Sacramento, CA, USA.
Sacramento VA Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The term spondyloarthritis (SpA) is used to describe a group of inflammatory autoimmune diseases, including ankylosing spondylitis and psoriatic arthritis, with common genetic risk factors and clinical features. SpA is clinically distinct from rheumatoid arthritis and typically affects the spine, sacroiliac joints, entheses, and, less commonly, peripheral joints. Although the pathogenesis of SpA is not fully understood, recent findings have identified the interleukin (IL)-17 pathway as a key mediator of disease pathogenesis. Clinical evidence for the efficacy of IL-17A inhibition by biologic agents was initially shown in patients with chronic plaque psoriasis, another autoimmune disease mediated by the IL-17 pathway. Subsequently, similar positive efficacy for inhibition of IL-17A was seen in patients with ankylosing spondylitis and psoriatic arthritis. Inhibition of IL-17A may also improve cardiovascular and metabolic comorbidities often found in patients with SpA because studies have linked these disorders to the IL-17 pathway. In this review, we will examine key preclinical studies that demonstrated the mechanistic role of IL-17A in the development SpA and discuss how these observations were translated into clinical practice.

Indexed as

HumansInterleukin-17SpondylarthropathiesInterleukin-17Ankylosing spondylitisClinical practiceIL-17A inhibitionInterleukin-17Preclinical studiesPsoriatic arthritisReviewSpondyloarthritis

Identifiers

PMID28270233
PMCPMC5341175
OpenAlexW2592004850

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.