Evidence map›Paper›PMID 25436214›Full record

ArticleJournal of immunology research2014

TNFα promotes Th17 cell differentiation through IL-6 and IL-1β produced by monocytes in rheumatoid arthritis.

Yingxia Zheng, Lei Sun, Ting Jiang, Dongqing Zhang, Dongyi He, Hong Nie

Open access · goldAbstract read
In one paragraph

Article in Journal of immunology research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.

0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

70 citing papers in PubMed, 101 citations in OpenAlex.

  1. Trial
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  4. Innate Immune Memory Responses in Organ Transplantation.Arteriosclerosis, thrombosis, and vascular biology · 2026
    Review
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  20. Observational

10 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

6 authors at 2 institutions in 1 country.

Yingxia ZhengShanghai Institute of Immunology, Institutes of Medical Sciences, Shanghai Jiao Tong University School of Medicine, 280 South Chongqing Road, Shanghai 200025, China ; Department of Clinical Laboratory, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, 1665 Kongjiang Road, Shanghai 200092, China.
Lei SunSchool of Pharmacy, Shanghai Jiao Tong University, 800 Dongchuan Road, Shanghai 200240, China.
Ting JiangGuanghua Integrative Medicine Hospital, 540 Xinhua Road, Shanghai 200052, China.
Dongqing ZhangShanghai Institute of Immunology, Institutes of Medical Sciences, Shanghai Jiao Tong University School of Medicine, 280 South Chongqing Road, Shanghai 200025, China.
Dongyi HeGuanghua Integrative Medicine Hospital, 540 Xinhua Road, Shanghai 200052, China ; Institute of Arthritis Research, Shanghai Academy of Chinese Medical Sciences, 540 Xinhua Road, Shanghai 200052, China.
Hong NieShanghai Institute of Immunology, Institutes of Medical Sciences, Shanghai Jiao Tong University School of Medicine, 280 South Chongqing Road, Shanghai 200025, China.ORCID 0000-0002-0038-6543
Shanghai Jiao Tong University · CNShanghai Guanghua Hospital of Integrated Traditional Chinese and Western Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

TNFα plays an important role in autoimmune pathogenesis and is the main therapeutic target of rheumatoid arthritis. However, its underlying mechanism is not completely understood. In this study, we described that Th17 cells were accumulated in synovial fluid, which was attributable to TNFα aberrantly produced in rheumatoid synovium. Interestingly, TNFα cannot induce IL-17 production of CD4(+) T cells directly, but through the monocytes high levels of IL-1β and IL-6 in a TNFRI and TNFRII dependent manner from the active RA patients are produced. TNFα was shown to enhance the phosphorylation level of STAT3 and the expression level of transcription factor RORC of CD4(+) T cells when cultured with CD14(+) monocytes. Treatment with an approved TNFα blocking antibody showed marked reduction in the levels of IL-6, IL-1β, and IL-17 and the expression level of STAT3 phosphorylation in relation to Th17 cell differentiation in patients with rheumatoid arthritis. The study provides new evidence supporting the critical role of TNFα in the pathogenic Th17 cell differentiation in rheumatoid arthritis.

Indexed as

AgedAntibodies, BlockingAntibodies, MonoclonalAntirheumatic AgentsArthritis, RheumatoidCD4-Positive T-LymphocytesCell DifferentiationCells, CulturedFemaleHumansImmunoblottingInfliximabInterleukin-1betaInterleukin-6MaleMiddle AgedAntibodies, BlockingAntibodies, MonoclonalAntirheumatic AgentsInfliximabInterleukin-1betaInterleukin-6Nuclear Receptor Subfamily 1, Group F, Member 3Receptors, Tumor Necrosis Factor, Type IReceptors, Tumor Necrosis Factor, Type IIRORC protein, humanSTAT3 Transcription FactorTumor Necrosis Factor-alpha

Identifiers

PMID25436214
PMCPMC4243768
OpenAlexW2071530841

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.