Evidence map›Paper›PMID 34350135›Full record

ReviewImmunoTargets and therapy2021

Contribution of Toll-Like Receptors and the NLRP3 Inflammasome in Rheumatoid Arthritis Pathophysiology.

Sarah Unterberger, Kevin A Davies, Srinivasa Bhargav Rambhatla, Sandra Sacre

Open access · goldAbstract readReview
In one paragraph

Review in ImmunoTargets and therapy, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.4field-weighted citation impact, top 10% 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

24 citing papers in PubMed, 43 citations in OpenAlex.

  1. Review
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  5. ACPA-Induced ATP release and KCell communication and signaling : CCS · 2025
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  19. Pannexin1 channels in the liver: an open enemy.Frontiers in cell and developmental biology · 2023
    Review
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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

4 authors at 1 institution in 1 country.

Sarah UnterbergerBrighton and Sussex Medical School, University of Sussex, Falmer, Brighton, BN1 9PS, UK.ORCID 0000-0002-1821-2859
Kevin A DaviesBrighton and Sussex Medical School, University of Sussex, Falmer, Brighton, BN1 9PS, UK.
Srinivasa Bhargav RambhatlaBrighton and Sussex Medical School, University of Sussex, Falmer, Brighton, BN1 9PS, UK.
Sandra SacreBrighton and Sussex Medical School, University of Sussex, Falmer, Brighton, BN1 9PS, UK.ORCID 0000-0003-1665-1142
Brighton and Sussex Medical School · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Rheumatoid arthritis (RA) is a progressive autoimmune disease that is characterized by inflammation of the synovial joints leading to cartilage and bone damage. The pathogenesis is sustained by the production of pro-inflammatory cytokines including tumor necrosis factor (TNF), interleukin (IL)-1 and IL-6, which can be targeted therapeutically to alleviate disease severity. Several innate immune receptors are suggested to contribute to the chronic inflammation in RA, through the production of pro-inflammatory factors in response to endogenous danger signals. Much research has focused on toll-like receptors and more recently the nucleotide-binding domain and leucine-rich repeat pyrin containing protein-3 (NLRP3) inflammasome, which is required for the processing and release of IL-1β. This review summarizes the current understanding of the potential involvement of these receptors in the initiation and maintenance of inflammation and tissue damage in RA and experimental arthritis models.

Indexed as

IL-1IL-6NLRP3 inflammasomerheumatoid arthritisTNFtoll-like receptor

Identifiers

PMID34350135
PMCPMC8326786
OpenAlexW3184848566

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.