Evidence map›Paper›PMID 25424423›Full record

ArticleImmunology2015

Toll-like receptor 8 deletion accelerates autoimmunity in a mouse model of lupus through a Toll-like receptor 7-dependent mechanism.

Ngoc Lan Tran, Céline Manzin-Lorenzi, Marie-Laure Santiago-Raber

Open access · bronzeAbstract read
In one paragraph

Article in Immunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
1.5field-weighted citation impact, top 18% 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

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 36 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Review
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  10. Article
  11. Article
  12. Targeting the innate immune receptor TLR8 using small-molecule agents.Acta crystallographica. Section D, Structural biology · 2020
    Review
  13. Sex-based differences in inflammatory bowel diseases: a review.Therapeutic advances in gastroenterology · 2020
    Review
  14. Review
  15. Review
  16. Human TLR8 Senses RNA FromFrontiers in immunology · 2019
    Article
  17. Article
  18. Review
  19. Review
  20. Roles of B Cell-Intrinsic TLR Signals in Systemic Lupus Erythematosus.International journal of molecular sciences · 2015
    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

3 authors at 1 institution in 1 country.

Ngoc Lan TranDepartment of Pathology and Immunology, Faculty of Medicine, University of Geneva, Geneva, Switzerland.
Céline Manzin-Lorenzi
Marie-Laure Santiago-Raber
University of Geneva · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Systemic lupus erythematosus is an autoimmune disorder characterized by increased levels of lymphocyte activation, antigen presentation by dendritic cells, and the formation of autoantibodies. This leads to immune complex-mediated glomerulonephritis. Toll-like receptor 7 (T7) and TLR9 localize to the endosomal compartment and play important roles in the generation of autoantibodies against nuclear components, as they recognize RNA and DNA, respectively. In contrast, very little is known about endogenous TLR8 activation in mice. We therefore tested whether TLR8 could affect autoimmune responses in a murine model of lupus. We introduced a Tlr8 null mutation into C57BL/6 mice congenic for the Nba2 (NZB autoimmunity 2) locus and bearing the Yaa (Y-linked autoimmune acceleration) mutation containing a tlr8 duplicated gene, and monitored disease development, autoantibody production, and glomerulonephritis-associated mortality. Cellular responses were investigated in female Nba2.TLR8(-/-) mice bearing no copy of tlr8. The TLR8 deficiency accelerated disease progression and mortality, increased the number of circulating antibodies and activated monocytes, and heightened cellular responses to TLR7 ligation. TLR8-deficient antigen-presenting cells exhibited increased levels of MHC class II expression. The ability of dendritic cells to present antigens to allogeneic T cells after TLR7 ligation was also improved by TLR8 deficiency. TLR8 deletion accelerated autoimmunity in lupus-prone mice in response to TLR7 activation. Antigen-presenting cell function seemed to play a key role in mediating the effects of TLR8 deficiency.

Indexed as

AnimalsAntibodies, AntinuclearDendritic CellsDisease Models, AnimalFemaleGene DeletionGene Expression RegulationHistocompatibility Antigens Class IILupus Erythematosus, SystemicMembrane GlycoproteinsMiceMice, KnockoutMonocytesToll-Like Receptor 7Toll-Like Receptor 8Antibodies, AntinuclearHistocompatibility Antigens Class IIMembrane GlycoproteinsTlr7 protein, mouseTLR8 protein, mouseToll-Like Receptor 7Toll-Like Receptor 8monocytessystemic lupus erythematosusToll-like receptors

Identifiers

PMID25424423
PMCPMC4405324
OpenAlexW2082856293

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.