Evidence map›Paper›PMID 26299984›Full record

ReviewAutoimmunity reviews2016

The critical role of toll-like receptors--From microbial recognition to autoimmunity: A comprehensive review.

Maximiliano Javier Jiménez-Dalmaroni, M Eric Gerswhin, Iannis E Adamopoulos

Open access · greenAbstract readComparative StudyReview
In one paragraph

Review in Autoimmunity reviews, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 128 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
128citing papers in PubMed, 5 pooled it
13.6field-weighted citation impact, top 1% 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

128 citing papers in PubMed, 5 syntheses or guidelines pooled it, 259 citations in OpenAlex.

  1. Pooled it
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  6. Trial
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  15. Research Progress on Anti-Inflammatory Mechanism ofInternational journal of molecular sciences · 2025
    Review
  16. Article
  17. Research progress in RBC alloimmunization.Frontiers in immunology · 2025
    Review
  18. Review
  19. Article
  20. Article

68 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.

Maximiliano Javier Jiménez-DalmaroniBiochemistry Research Institute of La Plata (INIBIOLP), Faculty of Medicine, National University of La Plata, La Plata, Argentina. Electronic address: mjimenez@med.unlp.edu.ar.
M Eric GerswhinDepartment of Internal Medicine, Division of Rheumatology, Allergy and Clinical Immunology, University of California at Davis School of Medicine, Davis, CA, 95616, USA.
Iannis E AdamopoulosDepartment of Internal Medicine, Division of Rheumatology, Allergy and Clinical Immunology, University of California at Davis School of Medicine, Davis, CA, 95616, USA; Institute for Pediatric Regenerative Medicine, Shriners Hospitals for Children Northern California, CA, 95817, USA. Electronic address: iannis@ucdavis.edu.
University of California, Davis · USBiochemistry Research Institute of La Plata · AR

Funding

The IL-23/IL-17 Axis in Inflammatory ArthritisR01AR062173 · NIAMS · UNIVERSITY OF CALIFORNIA AT DAVIS · PI LEVY, DAN · 2012 to 2025
$4.9M
NIAMS NIH HHS AR62173NIAMS NIH HHS R01 AR062173
6 · The paper itself

Abstract

Toll-like receptors (TLRs) constitute an important mechanism in the activation of innate immune cells including monocytes, macrophages and dendritic cells. Macrophage activation by TLRs is pivotal in the initiation of the rapid expression of pro-inflammatory cytokines TNF, IL-1β and IL-6 while promoting Th17 responses, all of which play critical roles in autoimmunity. Surprisingly, in inflammatory arthritis, activation of specific TLRs can not only induce but also inhibit cellular processes associated with bone destruction. The intercellular and intracellular orchestration of signals from different TLRs, their endogenous or microbial ligands and accessory molecules determine the activating or inhibitory responses. Herein, we review the TLR-mediated activation of innate immune cells in their activation and differentiation to osteoclasts and the capacity of these signals to contribute to bone destruction in arthritis. Detailed understanding of the opposing mechanisms of TLRs in the induction and suppression of cellular processes in arthritis may pave the way to develop novel therapies to treat autoimmunity.

Indexed as

AutoimmunityAnimalsArthritisB-LymphocytesHumansLigandsSignal TransductionTh17 CellsToll-Like ReceptorsLigandsToll-Like ReceptorsInnate immunityOsteoclastsRheumatoid arthritisToll-like receptors

Identifiers

PMID26299984
PMCPMC4679489
OpenAlexW1586581625

What OpenQuestion holds

Textmetadata
LicenceTDM
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.