Evidence map›Paper›PMID 20848219›Full record

ReviewMolecular biology reports2011

Targeting interleukin-21 in rheumatoid arthritis.

Feng-Lai Yuan, Wei Hu, Wei-Guo Lu, Xia Li, Jian-Ping Li, Rui-Sheng Xu, Cheng-Wan Li, Fei-Hu Chen, Cheng Jin

Abstract readReview
PubMed Publisher
In one paragraph

Review in Molecular biology reports, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 1 pooled it
1.5field-weighted citation impact, top 18% 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

28 citing papers in PubMed, 1 synthesis or guideline pooled it, 45 citations in OpenAlex.

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  7. Rheumatoid Arthritis: Pathogenic Roles of Diverse Immune Cells.International journal of molecular sciences · 2022
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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

9 authors at 3 institutions in 1 country.

Feng-Lai YuanThe Third Hospital Affiliated to Nantong University, Wuxi, 214041 Jiangsu, People's Republic of China.
Wei Hu
Wei-Guo Lu
Xia Li
Jian-Ping Li
Rui-Sheng Xu
Cheng-Wan Li
Fei-Hu Chen
Cheng Jin
Wuxi Third People's Hospital · CNAnhui Medical University · CNSecond Hospital of Anhui Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Interleukin-21 (IL-21) is a new member of the type I cytokine superfamily, which binds to a composite receptor that consists of a private receptor (IL-21R) and the common cytokine receptor γ chain. Recently, increasing evidence has shown that IL-21 contributes to the pathogenesis of chronic inflammatory and autoimmune diseases because of its pro-inflammatory and immune-mediated properties. IL-21 induced T-cell activation and pro-inflammatory cytokine secretion in rheumatoid arthritis (RA). IL-21R RNA transcripts were found in synovial tissue samples of patients with RA. In addition, blockade of the IL-21/IL-21R pathway ameliorated disease in animal models of RA and significantly inhibited inflammatory cytokine production in vitro. Moreover, IL-21R deficiency in the K/BxN mouse model of inflammatory arthritis was sufficient to block arthritis initiation completely. All theses findings suggest that IL-21 has important biological effects in autoimmunity that might be a promising therapeutic target for RA. In this review, we discuss the biological features of IL-21 and summarize recent advances in the role of IL-21 in the pathogenesis and treatment of RA.

Indexed as

AnimalsArthritis, RheumatoidHumansInterleukin-21InterleukinsReceptors, Interleukin-21Signal TransductionInterleukin-21InterleukinsReceptors, Interleukin-21

Identifiers

PMID20848219
OpenAlexW2081435557

What OpenQuestion holds

Textmetadata
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.