Evidence map›Paper›PMID 20886024›Full record

ReviewMediators of inflammation2010

Targeting Toll-like receptors for treatment of SLE.

Christopher G Horton, Zi-jian Pan, A Darise Farris

Open access · goldAbstract readReview
In one paragraph

Review in Mediators of inflammation, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

29 citing papers in PubMed, 60 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. EGF-Receptor-Dependent TLR7 Signaling in Macrophages Promotes Glomerular Injury in Crescentic Glomerulonephritis.Laboratory investigation; a journal of technical methods and pathology · 2023
    Article
  5. B Lineage Cells in ANCA-Associated Vasculitis.International journal of molecular sciences · 2021
    Review
  6. Toll-Like Receptor as a Potential Biomarker in Renal Diseases.International journal of molecular sciences · 2020
    Review
  7. Review
  8. Article
  9. TLR7-Mediated Lupus Nephritis Is Independent of Type I IFN Signaling.Journal of immunology (Baltimore, Md. : 1950) · 2018
    Article
  10. Article
  11. Article
  12. Article
  13. Critical role of RAGE and HMGB1 in inflammatory heart disease.Proceedings of the National Academy of Sciences of the United States of America · 2016
    Article
  14. Review
  15. Review
  16. Review
  17. Review
  18. Roles of B Cell-Intrinsic TLR Signals in Systemic Lupus Erythematosus.International journal of molecular sciences · 2015
    Review
  19. Review
  20. Article
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 1 institution in 1 country.

Christopher G HortonDepartment of Microbiology and Immunology, University of Oklahoma Health Sciences Center, Oklahoma City, OK 73104, USA.
Zi-jian Pan
A Darise Farris
Oklahoma Medical Research Foundation · US

Funding

SNP Confirmation and High Throughput Genotyping CoreP30AR053483 · NIAMS · OKLAHOMA MEDICAL RESEARCH FOUNDATION · PI GUTHRIDGE, JOEL MARVIN · 2007 to 2017
$6.7M
Molecular Basis of Immunity - Kirschtein-NRSAT32AI007633 · NIAID · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI CUNNINGHAM, MADELEINE W. · 2001 to 2022
$4.0M
T cell to tolerance &autoimmunity to nuclear antigen LaR01AI048097 · NIAID · OKLAHOMA MEDICAL RESEARCH FOUNDATION · PI FARRIS, A DARISE · 2001 to 2012
$2.3M
NIAID NIH HHS R01 AI048097NIAID NIH HHS T32 AI007633NIAMS NIH HHS P30 AR053483
6 · The paper itself

Abstract

Toll-like receptors (TLRs) are important innate immune receptors for the identification and clearance of invading pathogens. Twelve TLRs that recognize various conserved components of microorganisms are currently known. Among these, the endosomal TLRs 3, 7/8, and 9 recognize dsRNA, ssRNA, and CpG DNA, respectively. Nucleic acid-sensing TLRs, TLR 7 in particular, have been implicated in systemic lupus erythematosus (SLE) and are thought to exacerbate disease pathology. Activation of these TLRs results in the production of inflammatory cytokines and type I interferon. Genome-wide association studies, single nucleotide polymorphism analyses as well as experimental mouse models have provided evidence of TLR signaling involvement in SLE and other autoimmune diseases. Since activation of these receptor pathways promotes autoimmune phenotypes, inhibitory drugs that target these pathways constitute important new therapeutic strategies for the treatment of systemic autoimmunity.

Indexed as

AnimalsAutoimmune DiseasesGenome-Wide Association StudyHumansLupus Erythematosus, SystemicMiceModels, BiologicalToll-Like ReceptorsToll-Like Receptors

Identifiers

PMID20886024
PMCPMC2945668
OpenAlexW2086046139

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.