Evidence map›Paper›PMID 31552019›Full record

ArticleFrontiers in immunology2019

Lupus Autoimmunity and Metabolic Parameters Are Exacerbated Upon High Fat Diet-Induced Obesity Due to TLR7 Signaling.

Noël Hanna Kazazian, Yawen Wang, Annie Roussel-Queval, Laetitia Marcadet, Lionel Chasson, Caroline Laprie, Benoit Desnues, Jonathan Charaix, Magali Irla, Lena Alexopoulou

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
2.4field-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

35 citing papers in PubMed, 47 citations in OpenAlex.

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  5. Adipose tissue releases nucleosides.American journal of physiology. Cell physiology · 2026
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  16. T-betCell metabolism · 2022
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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

10 authors at 3 institutions in 1 country.

Noël Hanna KazazianAix Marseille University, CNRS, INSERM, CIML, Marseille, France.
Yawen WangAix Marseille University, CNRS, INSERM, CIML, Marseille, France.
Annie Roussel-QuevalAix Marseille University, CNRS, INSERM, CIML, Marseille, France.
Laetitia MarcadetAix Marseille University, CNRS, INSERM, CIML, Marseille, France.
Lionel ChassonAix Marseille University, CNRS, INSERM, CIML, Marseille, France.
Caroline LaprieAix Marseille University, CNRS, INSERM, CIML, Marseille, France.
Benoit DesnuesAix Marseille University, CNRS, INSERM, CIML, Marseille, France.
Jonathan CharaixAix Marseille University, CNRS, INSERM, CIML, Marseille, France.
Magali IrlaAix Marseille University, CNRS, INSERM, CIML, Marseille, France.
Lena AlexopoulouAix Marseille University, CNRS, INSERM, CIML, Marseille, France.
Inserm · FRCentre National de la Recherche Scientifique · FRAix-Marseille Université · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Systemic lupus erythematosus (SLE) patients have increased prevalence of metabolic syndrome but the underlying mechanisms are unknown. Toll-like receptor 7 (TLR7) that detects single stranded-RNA plays a key role in antimicrobial host defense and also contributes to the initiation and progression of SLE both in mice and humans. Here, we report the implication of TLR7 signaling in high fat diet (HFD)-induced metabolic syndrome and exacerbation of lupus autoimmunity in TLR8-deficient (TLR8ko) mice, which develop spontaneous lupus-like disease due to increased TLR7 signaling by dendritic cells (DCs). The aggravated SLE pathogenesis in HFD-fed TLR8ko mice was characterized by increased overall immune activation, anti-DNA autoantibody production, and IgG/IgM glomerular deposition that were coupled with increased kidney histopathology. Moreover, upon HFD TLR8ko mice developed metabolic abnormalities, including liver inflammation. In contrast, upon HFD TLR7/8ko mice did not develop SLE and both TLR7ko and TLR7/8ko mice were fully protected from metabolic abnormalities, including body weight gain, insulin resistance, and liver inflammation. Interestingly, HFD led to an increase of TLR7 expression in WT mice, that was coupled with increased TNF production by DCs, and this phenotype was more profound in TLR8ko mice. Our study uncovers the implication of TLR7 signaling in the interconnection of SLE and metabolic abnormalities, indicating that TLR7 might be a novel approach as a tailored therapy in SLE and metabolic diseases.

Indexed as

AnimalsAntibodies, AntinuclearDendritic CellsDiet, High-FatHumansInsulin ResistanceLupus Erythematosus, SystemicLymphocyte ActivationMice, Inbred C57BLMice, KnockoutObesitySignal TransductionToll-Like Receptor 7Toll-Like Receptor 8Weight GainAntibodies, AntinuclearToll-Like Receptor 7Toll-Like Receptor 8animal modeldendritic cellsinnate immunitymetabolic syndromeobesitysystemic lupus erythematosus (SLE)toll-like receptor 7 (TLR7)

Identifiers

PMID31552019
PMCPMC6738575
OpenAlexW2967458835

What OpenQuestion holds

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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.