Evidence map›Paper›PMID 38361527›Full record

ArticleFrontiers in immunology2023

The susceptibility of single nucleotide polymorphisms located within co-stimulatory pathways to systemic lupus erythematosus.

Ding-Ping Chen, Wei-Tzu Lin, Fang-Ping Hsu, Kuang-Hui Yu

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2023. 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
3.4field-weighted citation impact, top 8% 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, 14 citations in OpenAlex.

  1. Review
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  4. Mitochondria-associated programmed cell death in pancreatic β cell of T2DM.Apoptosis : an international journal on programmed cell death · 2026
    Review
  5. Applications of single-cell transcriptomics: updated insights in endometrial cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
    Review
  6. Review
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  11. Review
  12. Construction of a disulfidptosis-related glycolysis gene risk model to predict the prognosis and immune infiltration analysis of gastric adenocarcinoma.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2024
    Article
  13. Article
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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 2 institutions in 1 country.

Ding-Ping ChenDepartment of Laboratory Medicine, Linkou Chang Gung Memorial Hospital, Taoyuan, Taiwan.
Wei-Tzu LinDepartment of Laboratory Medicine, Linkou Chang Gung Memorial Hospital, Taoyuan, Taiwan.
Fang-Ping HsuDepartment of Laboratory Medicine, Linkou Chang Gung Memorial Hospital, Taoyuan, Taiwan.
Kuang-Hui YuDivision of Rheumatology, Allergy, and Immunology, Linkou Chang Gung University and Memorial Hospital, Taoyuan, Taiwan.
Linkou Chang Gung Memorial Hospital · TWChang Gung University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Introduction: Autoimmune diseases result from the loss of immune tolerance, and they exhibit complex pathogenic mechanisms that remain challenging to effectively treat. It has been reported that the altered expression levels of co-stimulatory/inhibitory molecules will affect the level of T/B cell activation and lead to the loss of immune tolerance. Methods: In this study, we evaluated the gene polymorphisms of the ligand genes corresponding co-stimulatory system that were expressed on antigen-presenting cells (CD80, CD86, ICOSLG, and PDL1) from 60 systemic lupus erythematosus (SLE) patients and 60 healthy controls. Results: The results showed that rs16829984 and rs57271503 of the CD80 gene and rs4143815 of the PDL1 gene were associated with SLE, in which the G-allele of rs16829984 (p=0.022), the A-allele of rs57271503 (p=0.029), and the GG and GC genotype of rs4143815 (p=0.039) may be risk polymorphisms for SLE. Discussion: These SNPs are in the promoter and 3'UTR of the genes, so they may affect the transcription and translation activity of the genes, thereby regulating immune function and contributing to the development of SLE.

Indexed as

Lupus Erythematosus, SystemicPolymorphism, Single NucleotideAllelesB7-1 AntigenGenotypeHumansB7-1 Antigen3 prime untranslated regioncostimulatory moleculesimmune regulatory genespromotersystemic lupus erythematosus

Identifiers

PMID38361527
PMCPMC10867627
OpenAlexW4391439075

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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.