Evidence map›Paper›PMID 26849368›Full record

Trial reportPloS one2016

Changes in Soluble CD18 in Murine Autoimmune Arthritis and Rheumatoid Arthritis Reflect Disease Establishment and Treatment Response.

Tue Wenzel Kragstrup, Babak Jalilian, Kresten Krarup Keller, Xianwei Zhang, Julie Kristine Laustsen, Kristian Stengaard-Pedersen, Merete Lund Hetland, Kim Hørslev-Petersen, Peter Junker, Mikkel Østergaard and 4 more

Open access · goldAbstract readRandomized Controlled Trial
In one paragraph

Trial report in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
2.2field-weighted citation impact, top 14% 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

11 citing papers in PubMed, 15 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Rheumatoid arthritis mediator CD18 expression byIranian journal of microbiology · 2019
    Article
  7. IL-12/IL-23p40 identified as a downstream target of apremilast inTherapeutic advances in musculoskeletal disease · 2019
    Article
  8. Article
  9. Review
  10. Article
  11. 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

14 authors at 6 institutions in 1 country.

Tue Wenzel KragstrupDepartment of Biomedicine, Aarhus University, Aarhus, Denmark.
Babak JalilianDepartment of Biomedicine, Aarhus University, Aarhus, Denmark.
Kresten Krarup KellerDepartment of Rheumatology, Aarhus University Hospital, Aarhus, Denmark.
Xianwei ZhangDepartment of Biomedicine, Aarhus University, Aarhus, Denmark.
Julie Kristine LaustsenDepartment of Biomedicine, Aarhus University, Aarhus, Denmark.
Kristian Stengaard-PedersenDepartment of Rheumatology, Aarhus University Hospital, Aarhus, Denmark.
Merete Lund HetlandCopenhagen Center for Arthritis Research, Rigshospitalet, Glostrup, Denmark.
Kim Hørslev-PetersenUniversity of Southern Denmark, Odense, Denmark.
Peter JunkerOdense University Hospital, Odense, Denmark.
Mikkel ØstergaardCopenhagen Center for Arthritis Research, Rigshospitalet, Glostrup, Denmark.
Ellen-Margrethe HaugeDepartment of Rheumatology, Aarhus University Hospital, Aarhus, Denmark.
Malene HvidDepartment of Biomedicine, Aarhus University, Aarhus, Denmark.
Thomas Vorup-JensenDepartment of Biomedicine, Aarhus University, Aarhus, Denmark.
Bent DeleuranDepartment of Biomedicine, Aarhus University, Aarhus, Denmark.
Aarhus University · DKAarhus University Hospital · DKGlostrup Hospital · DKOdense University Hospital · DKUniversity of Copenhagen · DKUniversity of Southern Denmark · DK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionIn rheumatoid arthritis (RA) immune activation and presence of autoantibodies may precede clinical onset of disease, and joint destruction can progress despite remission. However, the underlying temporal changes of such immune system abnormalities in the inflammatory response during treat-to-target strategies remain poorly understood. We have previously reported low levels of the soluble form of CD18 (sCD18) in plasma from patients with chronic RA and spondyloarthritis. Here, we study the changes of sCD18 before and during treatment of early RA and following arthritis induction in murine models of rheumatoid arthritis.

methodsThe level of sCD18 was analyzed with a time-resolved immunoflourometric assay in 1) plasma from early treatment naïve RA patients during a treat-to-target strategy (the OPERA cohort), 2) plasma from chronic RA patients, 3) serum from SKG and CIA mice following arthritis induction, and 4) supernatants from synovial fluid mononuclear cells (SFMCs) and peripheral blood mononuclear cells (PBMCs) from 6 RA patients cultured with TNFα or adalimumab.

resultsPlasma levels of sCD18 were decreased in chronic RA patients compared with early RA patients and in early RA patients compared with healthy controls. After 12 months of treatment the levels in early RA patients were similar to healthy controls. This normalization of plasma sCD18 levels was more pronounced in patients with very early disease who achieved an early ACR response. Plasma sCD18 levels were associated with radiographic progression. Correspondingly, the serum level of sCD18 was decreased in SKG mice 6 weeks after arthritis induction compared with healthy littermates. The sCD18 levels in both SKG and CIA mice exhibited a biphasic course after arthritis induction with an initial increase above baseline followed by a decline. Shedding of CD18 from RA SFMC and RA PBMC cultures was increased by TNFα and decreased by adalimumab.

conclusionsThe plasma sCD18 levels were altered in patients with RA, in mice with autoimmune arthritis and in cell cultures treated with TNFα and adalimumab. Decreased levels of plasma sCD18 could reflect autoimmunity in transition from early to chronic disease and normalization in response to treatment could reflect autoimmunity in remission.

Indexed as

AdalimumabAdultAnimalsAntirheumatic AgentsArthritis, RheumatoidCD18 AntigensChronic DiseaseDisease Models, AnimalFemaleHumansLeukocytes, MononuclearMaleMethotrexateMice, Inbred C57BLMice, Inbred StrainsMiddle AgedAdalimumabAntirheumatic AgentsCD18 AntigensMethotrexate

Identifiers

PMID26849368
PMCPMC4743942
OpenAlexW2264875245

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.