Evidence map›Paper›PMID 39896198›Full record

ArticleJournal of translational autoimmunity2025

Across ancestries, HLA-B∗08:01∼DRB1∗03:01 (DR3) and HLA-DQA∗01:02 (DR2) increase the risk to develop juvenile-onset systemic lupus erythematosus through low complement C4 levels.

Yves Renaudineau, Amandine Charras, Valentina Natoli, Nicolas Congy-Jolivet, Sam Haldenby, Xuan Liu, Yongxiang Fang, Eve Md Smith, Michael W Beresford, Christian M Hedrich and 1 more

Abstract read
In one paragraph

Article in Journal of translational autoimmunity, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
–field-weighted citation impact
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

6 citing papers in PubMed.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Divergent T Cell Phenotypes Define Pediatric Crohn's Disease and Ulcerative Colitis.medRxiv : the preprint server for health sciences · 2025
    Article
  6. 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

11 authors.

Yves RenaudineauImmunology Department Laboratory, Referral Medical Biology Laboratory, Institut Fédératif de Biologie, Toulouse University Hospital Centre, France.
Amandine CharrasDepartment of Women's & Children's Health, Institute of Life Course and Medical Sciences, University of Liverpool, United Kingdom.
Valentina NatoliDepartment of Women's & Children's Health, Institute of Life Course and Medical Sciences, University of Liverpool, United Kingdom.
Nicolas Congy-JolivetImmunology Department Laboratory, Referral Medical Biology Laboratory, Institut Fédératif de Biologie, Toulouse University Hospital Centre, France.
Sam HaldenbyCentre for Genomic Research, Shared Research Facilities, University of Liverpool, United Kingdom.
Xuan LiuCentre for Genomic Research, Shared Research Facilities, University of Liverpool, United Kingdom.
Yongxiang FangCentre for Genomic Research, Shared Research Facilities, University of Liverpool, United Kingdom.
Eve Md SmithDepartment of Women's & Children's Health, Institute of Life Course and Medical Sciences, University of Liverpool, United Kingdom.
Michael W BeresfordDepartment of Women's & Children's Health, Institute of Life Course and Medical Sciences, University of Liverpool, United Kingdom.
Christian M HedrichDepartment of Women's & Children's Health, Institute of Life Course and Medical Sciences, University of Liverpool, United Kingdom.
UK jSLE Cohort Study Group

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Objective: Systemic lupus erythematosus (SLE) is a systemic autoimmune/inflammatory disease with a strong genetic component. Genetic burden is higher in children when compared to patients with adult-onset SLE, contributing to earlier disease expression and more severe phenotypes. The human leukocyte antigen (HLA) cluster on chromosome 6p21.3 is among the most variable genomic regions, representing a major risk-factor for SLE in adults. Its impact on juvenile-onset (j)SLE remains largely unstudied. Methods: High-resolution sequencing of HLA class I (A, B, C), class II (DRB1, DQA1, DQB1) and class III (complement Results: Although important ancestral recombination was reported for HLA-DR2 and -DR3 haplotypes, risk associated with jSLE was conserved at related alleles (DR2h: DRB1∗15:01, DQA∗01:02, DQB1∗06:02; DR3h: C∗07:02 [Asian], B∗08:01, Conclusion: Genetic variation in the

Indexed as

C4ComplementDisease activityGeneticHaplotypeHLAJuvenile-onsetLupusSLE

Identifiers

PMID39896198
PMCPMC11786776

What OpenQuestion holds

Textmetadata
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.