Evidence map›Paper›PMID 28763101›Full record

ArticleClinical and experimental immunology2017

Relevant genetic polymorphisms and kidney expression of Toll-like receptor (TLR)-5 and TLR-9 in lupus nephritis.

N Elloumi, R Fakhfakh, O Abida, L Ayadi, S Marzouk, H Hachicha, M Fourati, Z Bahloul, M N Mhiri, K Kammoun and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Clinical and experimental immunology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

25 citing papers in PubMed, 38 citations in OpenAlex.

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  15. Targeting DAMPs with nucleic acid scavengers to treat lupus.Translational research : the journal of laboratory and clinical medicine · 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

11 authors at 1 institution in 1 country.

N ElloumiImmunology Department, Habib Bourguiba Hospital, University of Sfax, Sfax, Tunisia.ORCID 0000-0001-6154-5854
R FakhfakhImmunology Department, Habib Bourguiba Hospital, University of Sfax, Sfax, Tunisia.
O AbidaImmunology Department, Habib Bourguiba Hospital, University of Sfax, Sfax, Tunisia.
L AyadiAnatomopathology Department, Habib Bourguiba Hospital, University of Sfax, Sfax, Tunisia.
S MarzoukInternal Medicine Department, Hedi Chaker Hospital, University of Sfax, Sfax, Tunisia.
H HachichaImmunology Department, Habib Bourguiba Hospital, University of Sfax, Sfax, Tunisia.
M FouratiUrology Department, Habib Bourguiba Hospital, University of Sfax, Sfax, Tunisia.
Z BahloulInternal Medicine Department, Hedi Chaker Hospital, University of Sfax, Sfax, Tunisia.
M N MhiriUrology Department, Habib Bourguiba Hospital, University of Sfax, Sfax, Tunisia.
K KammounNephrology Department, Hedi Chaker Hospital, University of Sfax, Sfax, Tunisia.
H MasmoudiImmunology Department, Habib Bourguiba Hospital, University of Sfax, Sfax, Tunisia.
University of Sfax · TN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Toll-like receptor (TLR) genetic polymorphisms may modify their expression causing inflammatory disorders and influencing both susceptibility and severity of lupus erythematosus. We aim to determine whether TLR-5 and TLR-9 gene polymorphisms are implicated in the susceptibility to systemic lupus erythematosus (SLE) and lupus nephritis (LN) and to evaluate their expressions and distributions in renal LN patients' biopsies. The frequencies of two SNP in the TLR-9 gene and one in the TLR-5 gene was examined in 106 SLE patients (among them 37 LN patients) and in 200 matched controls by polymerase chain reaction-restriction fragment-length polymorphisms (PCR-RFLP) analysis. TLR-9 and TLR-5 expressions were assessed by reverse transcription (RT)-PCR and immunohistochemistry carried on LN renal biopsies compared to healthy renal tissue. A significant genotypic and allelic association was revealed between TLR-9-rs352140 and both SLE and LN (P < 0·05). The TLR-9 transcript level was significantly higher in LN biopsies compared to control (P < 0·05). This increase was observed histochemically in the tubulointerstitial compartment. TLR-9 was detectable in LN glomeruli patients but not in normal control glomeruli. No allelic nor genotype association was found with TLR-5-rs5744168 in SLE. but the T allele and the TT genotype were raised significantly in the LN group (P < 0·05). A significant increase in TLR-5 gene expression in LN biopsies, which contrasted with normal kidneys (P < 0·05), was confirmed by an intense and diffuse staining for TLR-5 only in LN tubules (P < 0·05). Our data show that TLR-5 and TLR-9 are susceptible genes to LN and that their expression is dysregulated in LN patients' kidneys, supporting a role of these mediators in the pathogenesis of LN.

Indexed as

Genetic Predisposition to DiseaseKidneyLupus NephritisToll-Like Receptor 5Toll-Like Receptor 9BiopsyCase-Control StudiesFemaleGene Expression RegulationHumansMalePolymorphism, Restriction Fragment LengthTLR5 protein, humanTLR9 protein, humanToll-Like Receptor 5Toll-Like Receptor 9autoimmunityinflammationToll-like receptors (TLRs)

Identifiers

PMID28763101
PMCPMC5680057
OpenAlexW2765857895

What OpenQuestion holds

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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.