Evidence map›Paper›PMID 17185327›Full record

ArticleAnnals of the rheumatic diseases2007

Persistence of interleukin 7 activity and levels on tumour necrosis factor alpha blockade in patients with rheumatoid arthritis.

Joel A G van Roon, Sarita A Y Hartgring, Marion Wenting-van Wijk, Kim M G Jacobs, Paul-Peter Tak, Johannes W J Bijlsma, Floris P J G Lafeber

Open access · bronzeAbstract read
In one paragraph

Article in Annals of the rheumatic diseases, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
3.0field-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

17 citing papers in PubMed, 49 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Interleukin-7 Induces Osteoclast FormationFrontiers in immunology · 2017
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  15. Review
  16. Evidence that cytokines play a role in rheumatoid arthritis.The Journal of clinical investigation · 2008
    Review
  17. 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

7 authors at 3 institutions in 1 country.

Joel A G van RoonDepartment of Rheumatology and Clinical Immunology, University Medical Center Utrecht, PO Box 85500, 3508 GA Utrecht, The Netherlands. J.vanRoon@umcutrecht.nl
Sarita A Y Hartgring
Marion Wenting-van Wijk
Kim M G Jacobs
Paul-Peter Tak
Johannes W J Bijlsma
Floris P J G Lafeber
University Medical Center Utrecht · NLAcademic Medical Center · NLUtrecht University · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesTo identify the mechanism of interleukin (IL)7-stimulated tumour necrosis factor alpha (TNFalpha) production and to determine the relationship between intra-articular IL7 and TNFalpha expression levels in patients with rheumatoid arthritis (RA). In addition, the effect of TNFalpha blockade on IL7 activity and on IL7 levels was studied.

methodsThe effect of IL7 on isolated CD4 T cells and CD14 monocytes/macrophages was studied. IL7 and TNFalpha levels were measured in the synovial fluid of patients with RA. In RA synovial tissue, IL7 and TNFalpha expression was assessed in addition to IL1beta, numbers of inflammatory cells and adhesion molecule expression. The extent to which TNFalpha blockade could prevent IL7-induced lymphocyte responses was studied in vitro. In addition, regulation of serum IL7 levels on anti-TNFalpha therapy (adalimumab) was studied.

resultsIL7 induced cell contact-dependent TNFalpha production by cocultures of T cells and monocytes, but not by T cells and monocytes cultured separately. IL7 and TNFalpha levels in RA synovial fluid and synovial tissue significantly correlated. IL7-stimulated lymphocyte responses were not inhibited by TNFalpha blockade. Circulating IL7 levels were significantly reduced in patients who successfully responded to anti-TNFalpha treatment. However, IL7 levels persisted in non-responders.

conclusionThe present data suggest that IL7 is an important inducer of T cell-dependent TNFalpha production in RA joints. This may contribute to the correlation of intra-articular IL7 and TNFalpha in these joints. Furthermore, the persistence of IL7-induced inflammatory activity on TNFalpha blockade in vitro and persistence of IL7 levels and disease activity in anti-TNFalpha non-responders suggest that IL7 might additionally promote TNFalpha-independent inflammation.

Indexed as

AdalimumabAntibodies, MonoclonalAntibodies, Monoclonal, HumanizedAnti-Inflammatory AgentsArthritis, RheumatoidCD4-Positive T-LymphocytesCell DivisionCells, CulturedFemaleHumansInterleukin-7Interleukin-7 Receptor alpha SubunitLymphocyte ActivationMacrophagesMaleMiddle AgedAdalimumabAntibodies, MonoclonalAntibodies, Monoclonal, HumanizedAnti-Inflammatory AgentsInterleukin-7Interleukin-7 Receptor alpha SubunitTumor Necrosis Factor-alpha

Identifiers

PMID17185327
PMCPMC1954618
OpenAlexW1967353266

What OpenQuestion holds

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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.