Evidence map›Paper›PMID 25687121›Full record

ReviewClinical reviews in allergy & immunology2016

Toll-Like Receptor Pathways in Autoimmune Diseases.

Ji-Qing Chen, Peter Szodoray, Margit Zeher

Abstract readReview
PubMed Publisher
In one paragraph

Review in Clinical reviews in allergy & immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 156 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
156citing papers in PubMed, 1 pooled it
6.9field-weighted citation impact, top 2% 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

156 citing papers in PubMed, 1 synthesis or guideline pooled it, 319 citations in OpenAlex.

  1. Pooled it
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  20. The Integrated Cellular and Molecular Landscape of Autoimmunity.bioRxiv : the preprint server for biology · 2025
    Article

96 more citing papers are in PubMed but not listed here.

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

3 authors at 2 institutions in 2 countries.

Ji-Qing ChenDivision of Clinical Immunology, Institute of Medicine, University of Debrecen, Moricz Zs. str. 22., H-4032, Debrecen, Hungary.
Peter SzodorayCentre for Immune Regulation, Department of Immunology, University of Oslo, Oslo University Hospital, Rikshospitalet, Oslo, Norway.
Margit ZeherDivision of Clinical Immunology, Institute of Medicine, University of Debrecen, Moricz Zs. str. 22., H-4032, Debrecen, Hungary. zeher@iiibel.dote.hu.
Oslo University Hospital · NOUniversity of Debrecen · HU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autoimmune diseases are a family of chronic systemic inflammatory disorders, characterized by the dysregulation of the immune system which finally results in the break of tolerance to self-antigen. Several studies suggest that Toll-like receptors (TLRs) play an essential role in the pathogenesis of autoimmune diseases. TLRs belong to the family of pattern recognition receptors (PRRs) that recognize a wide range of pathogen-associated molecular patterns (PAMPs). TLRs are type I transmembrane proteins and located on various cellular membranes. Two main groups have been classified based on their location; the extracelluar group referred to the ones located on the plasma membrane while the intracellular group all located in endosomal compartments responsible for the recognition of nucleic acids. They are released by the host cells and trigger various intracellular pathways which results in the production of proinflammatory cytokines, chemokines, as well as the expression of co-stimulatory molecules to protect against invading microorganisms. In particular, TLR pathway-associated proteins, such as IRAK, TRAF, and SOCS, are often dysregulated in this group of diseases. TLR-associated gene expression profile analysis together with single nucleotide polymorphism (SNP) assessment could be important to explain the pathomechanism driving autoimmune diseases. In this review, we summarize recent findings on TLR pathway regulation in various autoimmune diseases, including Sjögren's syndrome (SS), systemic lupus erythematosus (SLE), multiple sclerosis (MS), rheumatoid arthritis (RA), systemic sclerosis (SSc), and psoriasis.

Indexed as

Signal TransductionAnimalsAutoimmune DiseasesCarrier ProteinsGenetic Predisposition to DiseaseHumansMultigene FamilyPolymorphism, Single NucleotideProtein BindingToll-Like ReceptorsCarrier ProteinsToll-Like ReceptorsAutoimmune diseaseIL-1-receptor-associated kinase (IRAK)Suppressor of cytokine signaling (SOCS)TNF-receptor-associated factor (TRAF)Toll-like receptors (TLRs)

Identifiers

PMID25687121
OpenAlexW2075494813

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.