Evidence map›Paper›PMID 33098626›Full record

ArticleImmunity, inflammation and disease2020

Low dose IL-2 suppress osteoclastogenesis in collagen-induced arthritis via JNK dependent pathway.

Han Sun, Yong Zhao, Kun Wang, Li Zhu, Jian Dong, Jie Zhao, Yimin Wang, Huan Li, Xiaoliang Sun, Yunjie Lu

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Immunity, inflammation and disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.5field-weighted citation impact, top 37% 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

9 citing papers in PubMed, 10 citations in OpenAlex.

  1. REJENERAInflammopharmacology · 2026
    Article
  2. Review
  3. The Role of Cytokines in Orthodontic Tooth Movement.International journal of molecular sciences · 2025
    Review
  4. Article
  5. Review
  6. Corrigendum.Immunity, inflammation and disease · 2022
    Article
  7. Article
  8. Review
  9. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 3 institutions in 1 country.

Han SunThe Third Affiliated Hospital of Soochow University, Changzhou, China.
Yong ZhaoDepartment of Hepatobiliary Surgery, The people's hospital of Jinsha County, China.
Kun WangThe Third Affiliated Hospital of Soochow University, Changzhou, China.
Li ZhuThe Third Affiliated Hospital of Soochow University, Changzhou, China.
Jian DongDepartment of Sports Medicine and Adult Reconstructive Surgery, Nanjing Drum Tower Hospital, The Affiliated Hospital of Nanjing University Medical School, China.
Jie ZhaoThe Third Affiliated Hospital of Soochow University, Changzhou, China.
Yimin WangThe Third Affiliated Hospital of Soochow University, Changzhou, China.
Huan LiThe Third Affiliated Hospital of Soochow University, Changzhou, China.
Xiaoliang SunThe Third Affiliated Hospital of Soochow University, Changzhou, China.
Yunjie LuThe Third Affiliated Hospital of Soochow University, Changzhou, China.ORCID 0000-0002-5786-717X
Soochow University · CNFourth People’s Hospital of Jinan · CNNanjing Drum Tower Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundRheumatoid arthritis (RA) is one of the most common chronic immune joint diseases, mainly involving blood vessels and small joints. The complex pathogenesis of RA greatly increases the difficulty of treatment. At present, the common hormone and immunosuppressive therapy are not effective, while low-dose interleukin-2 (IL-2) recently has been found to possess some advantages for immunotherapy. However, its related signal pathway remains to be elucidated.

methodsWe fabricated the model of arthritis in mice, and then low-dose IL-2 was injected at a fixed time point to observe the changes of related vascular and organ pathology, inflammatory factors, and signal pathway proteins, which were verified by statistical analysis.

resultsLow dose IL-2 can reduce the severity of vascular and bone lesions in collagen-induced arthritis immune model, and inhibit osteoclast formation in vitro by phosphorylation of nuclear factor-κB (NF-κB), which inhibits the receptor activator of NF-κB ligand effect through c-Jun N-terminal kinase (JNK) pathway, and its immunotherapeutic effect depends on the activation of JNK.

conclusionIt is the first time for us to prove that low dose IL-2 can inhibit osteoclast formation in collagen-induced arthritis through the JNK dependent pathway, which will provide the angle and theoretical basis for future immunotherapy of IL-2.

Indexed as

Arthritis, ExperimentalOsteogenesisAnimalsFemaleInterleukin-2MiceMice, Inbred DBAOsteoclastsInterleukin-2c-Jun N-terminal kinasecollagen-induced arthritisinterleukin-2NF-κBrheumatoid arthritis

Identifiers

PMID33098626
PMCPMC7654429
OpenAlexW3094330494

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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.