Evidence map›Paper›PMID 24352680›Full record

ReviewClinical reviews in allergy & immunology2014

TLR2 and TLR4 in autoimmune diseases: a comprehensive review.

Yu Liu, Heng Yin, Ming Zhao, Qianjin Lu

Abstract readReview
PubMed Publisher
In one paragraph

Review in Clinical reviews in allergy & immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 196 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
196citing papers in PubMed, 3 pooled it
9.0field-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

196 citing papers in PubMed, 3 syntheses or guidelines pooled it, 365 citations in OpenAlex.

  1. Pooled it
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  4. Impact ofInternational journal of molecular sciences · 2026
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  9. Therapeutic Potential ofLife (Basel, Switzerland) · 2025
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136 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

4 authors at 3 institutions in 1 country.

Yu LiuDepartment of Dermatology, Second Xiangya Hospital, Central South University, #139 Renmin Middle Rd, Changsha, Hunan, 410011, People's Republic of China.
Heng Yin
Ming Zhao
Qianjin Lu
Changsha Medical University · CNCentral South University · CNSecond Xiangya Hospital of Central South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autoimmune diseases are immune disorders characterized by T cell hyperactivity and B cell overstimulation leading to overproduction of autoantibodies. Although the pathogenesis of various autoimmune diseases remains to be elucidated, environmental factors have been thought to contribute to the initiation and maintenance of auto-respond inflammation. Toll-like receptors (TLRs) are pattern recognition receptors belonging to innate immunity that recognize and defend invading microorganisms. Besides these exogenous pathogen-associated molecular patterns, TLRs can also bind with damage-associated molecular patterns produced under strike or by tissue damage or cells apoptosis. It is believed that TLRs build a bridge between innate immunity and autoimmunity. There are five adaptors to TLRs including MyD88, TRIF, TIRAP/MAL, TRAM, and SARM. Upon activation, TLRs recruit specific adaptors to initiate the downstream signaling pathways leading to the production of inflammatory cytokines and chemokines. Under certain circumstances, ligation of TLRs drives to aberrant activation and unrestricted inflammatory responses, thereby contributing to the perpetuation of inflammation in autoimmune diseases. In the past, most studies focused on the intracellular TLRs, such as TLR3, TLR7, and TLR9, but recent studies reveal that cell surface TLRs, especially TLR2 and TLR4, also play an essential role in the development of autoimmune diseases and afford multiple therapeutic targets. In this review, we summarized the biological characteristics, signaling mechanisms of TLR2/4, the negative regulators of TLR2/4 pathway, and the pivotal function of TLR2/4 in the pathogenesis of autoimmune diseases including rheumatoid arthritis, systemic lupus erythematosus, systemic sclerosis, Sjogren's syndrome, psoriasis, multiple sclerosis, and autoimmune diabetes.

Indexed as

Adaptor Proteins, Signal TransducingAutoantibodiesAutoimmune DiseasesAutoimmunityB-LymphocytesCytokinesGene-Environment InteractionGene Expression RegulationHumansImmunity, InnateSignal TransductionT-LymphocytesToll-Like Receptor 2Toll-Like Receptor 4Adaptor Proteins, Signal TransducingAutoantibodiesCytokinesTLR2 protein, humanTLR4 protein, humanToll-Like Receptor 2Toll-Like Receptor 4

Identifiers

PMID24352680
OpenAlexW2118968734

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.