Evidence map›Paper›PMID 28278279›Full record

ArticlePloS one2017

Toll-like receptor 9 suppresses lupus disease in Fas-sufficient MRL Mice.

Kevin M Nickerson, Yujuan Wang, Sheldon Bastacky, Mark J Shlomchik

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.7field-weighted citation impact, top 17% 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

21 citing papers in PubMed, 27 citations in OpenAlex.

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  13. B cell-intrinsic TLR9 expression is protective in murine lupus.The Journal of clinical investigation · 2020
    Article
  14. Review
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  18. Kidney Proximal Tubular TLR9 Exacerbates Ischemic Acute Kidney Injury.Journal of immunology (Baltimore, Md. : 1950) · 2018
    Article
  19. Review
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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 1 institution in 1 country.

Kevin M NickersonDepartment of Immunology, University of Pittsburgh, Pittsburgh, Pennsylvania, United States of America.ORCID http://orcid.org/0000-0002-0114-2671
Yujuan WangDepartment of Immunology, University of Pittsburgh, Pittsburgh, Pennsylvania, United States of America.
Sheldon BastackyDepartment of Pathology, University of Pittsburgh, Pittsburgh, Pennsylvania, United States of America.
Mark J ShlomchikDepartment of Immunology, University of Pittsburgh, Pittsburgh, Pennsylvania, United States of America.
University of Pittsburgh · US

Funding

Toll-Like Receptors in Systemic Autoimmune DiseaseP01AR050256 · NIAMS · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI SHLOMCHIK, MARK J · 2004 to 2013
$13.4M
Single Nephron and MetabolomicsP30DK079307 · NIDDK · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI KLEYMAN, THOMAS R · 2008 to 2022
$13.4M
Investigating How TLR7 Activates and TLR9 Regulates Systemic AutoimmunityR37AI118841 · NIAID · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI SHLOMCHIK, MARK J · 2016 to 2025
$4.2M
Mechanisms of Autoimmune Activation and Regulation by Innate Immune ReceptorsR01AI084958 · NIAID · YALE UNIVERSITY · PI SHLOMCHIK, MARK J · 2010 to 2014
$702k
NIAID NIH HHS R01 AI084958NIAID NIH HHS R37 AI118841NIAMS NIH HHS P01 AR050256NIDDK NIH HHS P30 DK079307
6 · The paper itself

Abstract

Genetic deficiency in TLR9 accelerates pathogenesis in the spontaneous polygenic MRL.Faslpr murine model of systemic lupus erythematosus, despite the absence of anti-nucleosome autoantibodies. However, it could be argued that this result was dependent on Fas-deficiency rather than lupus-promoting genes in the MRL genetic background. Here we report the effects of TLR9 deficiency on autoimmune disease independent of the lpr mutation in Fas by characterizing Tlr9-/- and Tlr9+/+ mice on the Fas-intact MRL/+ genetic background. By 30 weeks of age, Tlr9-deficient MRL/+ had more severe renal disease, increased T cell activation, and higher titers of anti-Sm and anti-RNA autoantibodies than Tlr9-intact animals, as had been the case in the MRL.Faslpr model. In addition, Tlr9-deficient MRL/+ mice had increased numbers of germinal center phenotype B cells and an increase in splenic neutrophils and conventional dendritic cell populations. Thus, the disease accelerating effects of Tlr9 deficiency are separable from those mediated by the Fas mutation in the lupus-prone MRL genetic background. Nonetheless, disease acceleration in Tlr9-deficient MRL/+ mice was phenotypically distinct from that in Fas-deficient counterparts, which has important implications.

Indexed as

AnimalsAutoantibodiesfas ReceptorFemaleLupus Erythematosus, SystemicMiceMice, Inbred MRL lprMutationToll-Like Receptor 9Autoantibodiesfas ReceptorToll-Like Receptor 9

Identifiers

PMID28278279
PMCPMC5344451
OpenAlexW2593376712

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Registered trials

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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.