Evidence map›Paper›PMID 30622982›Full record

ReviewJournal of immunology research2018

Neutrophil Function in an Inflammatory Milieu of Rheumatoid Arthritis.

Weiqian Chen, Qin Wang, Yini Ke, Jin Lin

Open access · goldAbstract readReview
In one paragraph

Review in Journal of immunology research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
3.4field-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

47 citing papers in PubMed, 74 citations in OpenAlex.

  1. Article
  2. Dual regulation of antiviral IFN response byJournal of pharmaceutical analysis · 2026
    Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Virtual Probing on the Influence of CaCell biochemistry and biophysics · 2025
    Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. [Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2024
    Article
  13. Review
  14. Article
  15. Review
  16. An ElevatedCurrent issues in molecular biology · 2024
    Article
  17. DNA hypomethylation ameliorates erosive inflammatory arthritis by modulating interferon regulatory factor-8.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  18. Article
  19. Review
  20. 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

4 authors at 1 institution in 1 country.

Weiqian ChenDivision of Rheumatology, First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, Zhejiang, China.
Qin WangDivision of Rheumatology, First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, Zhejiang, China.
Yini KeDivision of Rheumatology, First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, Zhejiang, China.
Jin LinDivision of Rheumatology, First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, Zhejiang, China.ORCID 0000-0002-0978-0723
Zhejiang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Rheumatoid arthritis (RA) is an inflammatory autoimmune disease characterized by the presence of autoantibodies against citrullinated protein antigens and proinflammatory cytokines which cause chronic synovitis, bone erosion, and eventual deformity; however, the precise etiology of RA is unclear. In the early stage of RA, neutrophils migrate into the articular cavity, become activated, and exert their function in an inflammatory process, suggesting an essential role of neutrophils in the initial events contributing to the pathogenesis of RA. Solid evidence exists that supports the contribution of neutrophil extracellular traps (NETs) to the production of autoantibodies against citrullinated proteins which can trigger the immune reaction in RA. Concurrently, proinflammatory cytokines regulate the neutrophil migration, apoptosis, and NET formation. As a result, the inflammatory neutrophils produce more cytokines and influence other immune cells thereby perpetuating the inflammatory condition in RA. In this review, we summarize the advances made in improving our understanding of neutrophil migration, apoptosis, and NET formation in the presence of an RA inflammatory milieu. We will also discuss the most recent strategies in modulating the inflammatory microenvironment that have an impact on neutrophil function which may provide alternative novel therapies for RA.

Indexed as

AnimalsApoptosisArthritis, RheumatoidCellular MicroenvironmentExtracellular TrapsHumansImmune System DiseasesImmunomodulationInflammationLeukocyte DisordersNeutrophils

Identifiers

PMID30622982
PMCPMC6304923
OpenAlexW2902102863

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.