Evidence map›Paper›PMID 34530864›Full record

ArticleJournal of translational medicine2021

IL-18 binding protein suppresses IL-17-induced osteoclastogenesis and rectifies type 17 helper T cell / regulatory T cell imbalance in rheumatoid arthritis.

Hong Ki Min, Sehee Kim, Ji-Yeon Lee, Kyoung-Woon Kim, Sang-Heon Lee, Hae-Rim Kim

Open access · goldAbstract read
In one paragraph

Article in Journal of translational medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
1.7field-weighted citation impact, top 15% 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

23 citing papers in PubMed, 1 synthesis or guideline pooled it, 33 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. The Roles of Interleukin-18 in Inflammation and Autoimmune Disease.Clinical reviews in allergy & immunology · 2026
    Review
  4. Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Programmed Cell Death in Rheumatoid Arthritis.Journal of inflammation research · 2025
    Review
  10. Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
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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.

Hong Ki MinDivision of Rheumatology, Department of Internal Medicine, Konkuk University Medical Center, Seoul, 05030, Republic of Korea.
Sehee KimDivision of Rheumatology, Department of Internal Medicine, Konkuk University Medical Center, Seoul, 05030, Republic of Korea.
Ji-Yeon LeeThe Rheumatism Research Center, Research Institute of Medical Science, Konkuk University School of Medicine, Seoul, 05030, Republic of Korea.
Kyoung-Woon KimR&D Center, OncoInsight, Seoul, 06373, Republic of Korea.
Sang-Heon LeeDivision of Rheumatology, Department of Internal Medicine, Research Institute of Medical Science, Konkuk University School of Medicine, Seoul, 05030, Republic of Korea.
Hae-Rim KimDivision of Rheumatology, Department of Internal Medicine, Research Institute of Medical Science, Konkuk University School of Medicine, Seoul, 05030, Republic of Korea. kimhaerim@kuh.ac.kr.
Konkuk University · KRKonkuk University Medical Center · KR

Funding

Ministry of Education NRF-2021R1A2C1010075
6 · The paper itself

Abstract

backgroundPatients with rheumatoid arthritis (RA) have increased levels of interleukin-18 (IL-18) and decreased levels of IL-18 binding protein (IL-18BP) in the serum and synovial fluid (SF) compared to those in patients with osteoarthritis (OA) or in healthy controls. In this study, we evaluated the effects of IL-18BP on osteoclastogenesis and T cell differentiation in RA in vitro.

methodsSerum and SF of patients with RA and OA were collected to compare IL-18 and IL-18BP levels by the enzyme-linked immunosorbent assay. Peripheral blood mononuclear cells (PBMCs) and SF mononuclear cells (SFMCs) of RA patients were cultured under type 17 helper T cell (Th17) polarisation conditions with or without IL-18BP. In addition, PBMCs were cultured in the presence of receptor activator of nuclear factor kappa-Β ligand (RANKL) or IL-17A with or without IL-18BP, and tartrate-resistant acid phosphatase (TRAP) staining and real-time quantitative polymerase chain reaction for expression levels of osteoclast-related genes were performed.

resultsIL-18 levels were higher in the serum and SF of patients with RA, whereas IL-18BP was lower in the SF of patients with RA than in the control group. Treatment of patients' PBMCs with IL-18BP decreased the differentiation of CD4

conclusionWe showed that IL-18BP can rectify the Th17/Treg imbalance and decrease IL-17-induced osteoclastogenesis in PBMCs from patients with RA. Therefore, IL-18BP may have therapeutic potential for RA treatment.

Indexed as

Arthritis, RheumatoidInterleukin-17Cells, CulturedHumansIntercellular Signaling Peptides and ProteinsLeukocytes, MononuclearOsteoclastsOsteogenesisRANK LigandTh17 CellsT-Lymphocytes, RegulatoryIntercellular Signaling Peptides and ProteinsInterleukin-17interleukin-18 binding proteinRANK LigandInterleukin-18 binding proteinOsteoclastogenesisRegulatory T cellRheumatoid arthritisType 17 helper T cell

Identifiers

PMID34530864
PMCPMC8444577
OpenAlexW3201269626

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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.