Evidence map›Paper›PMID 29687651›Full record

ArticleArthritis & rheumatology (Hoboken, N.J.)2018

Toll-Like Receptor 9 Deficiency Breaks Tolerance to RNA-Associated Antigens and Up-Regulates Toll-Like Receptor 7 Protein in Sle1 Mice.

Teja Celhar, Hiroko Yasuga, Hui Yin Lee, Olga Zharkova, Shubhita Tripathi, Susannah I Thornhill, Hao K Lu, Bijin Au, Lina H K Lim, Thomas P Thamboo and 4 more

Open access · hybridAbstract read
In one paragraph

Article in Arthritis & rheumatology (Hoboken, N.J.), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.7field-weighted citation impact, top 33% 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

14 citing papers in PubMed, 17 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Rosmarinic Acid AttenuatesAntioxidants (Basel, Switzerland) · 2024
    Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. The Role of Nucleic Acid Sensing in Controlling Microbial and Autoimmune Disorders.International review of cell and molecular biology · 2019
    Review
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

14 authors at 5 institutions in 3 countries.

Teja CelharSingapore Immunology Network, Agency for Science, Technology, and Research, Singapore.
Hiroko YasugaSingapore Immunology Network, Agency for Science, Technology, and Research, Singapore.
Hui Yin LeeSingapore Immunology Network, Agency for Science, Technology, and Research, Singapore.
Olga ZharkovaSingapore Immunology Network, Agency for Science, Technology, and Research, Singapore.
Shubhita TripathiSingapore Immunology Network, Agency for Science, Technology, and Research, Singapore.
Susannah I ThornhillSingapore Immunology Network, Agency for Science, Technology, and Research, Singapore.
Hao K LuSingapore Immunology Network, Agency for Science, Technology, and Research, Singapore.
Bijin AuInstitute of Molecular and Cell Biology, Agency for Science, Technology, and Research, Singapore.
Lina H K LimNational University Hospital, Singapore.
Thomas P ThambooNational University Hospital, Singapore.
Shizuo AkiraOsaka University, Osaka, Japan.
Edward K WakelandUniversity of Texas Southwestern Medical Center, Dallas.
John E ConnollyInstitute of Molecular and Cell Biology, Agency for Science, Technology, and Research, Singapore.
Anna-Marie FairhurstSingapore Immunology Network, Agency for Science, Technology, and Research, Singapore.
Agency for Science, Technology and Research · SGSingapore Immunology Network · SGNational University Hospital · SGOsaka University · JPThe University of Texas Southwestern Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveToll-like receptors (TLRs) 7 and 9 are important innate signaling molecules with opposing roles in the development and progression of systemic lupus erythematosus (SLE). While multiple studies support the notion of a dependency on TLR-7 for disease development, genetic ablation of TLR-9 results in severe disease with glomerulonephritis (GN) by a largely unknown mechanism. This study was undertaken to examine the suppressive role of TLR-9 in the development of severe lupus in a mouse model.

methodsWe crossed Sle1 lupus-prone mice with TLR-9-deficient mice to generate Sle1TLR-9

resultsSle1TLR-9

conclusionThe increase in TLR-7-reactive immune complexes, and the concomitant enhanced expression of their receptor, promotes inflammation and disease in Sle1TLR9

Indexed as

AnimalsAntigensDisease Models, AnimalLupus Erythematosus, SystemicLupus NephritisMiceRNAToll-Like Receptor 7Toll-Like Receptor 9Up-RegulationAntigensRNAToll-Like Receptor 7Toll-Like Receptor 9

Identifiers

PMID29687651
PMCPMC6175219
OpenAlexW2801708452

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.