Evidence map›Paper›PMID 35149194›Full record

ArticleClinical immunology (Orlando, Fla.)2022

Systemic lupus erythematosus as a genetic disease.

Isaac T W Harley, Amr H Sawalha

Open access · greenAbstract read
In one paragraph

Article in Clinical immunology (Orlando, Fla.), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
8.9field-weighted citation impact, top 2% 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

33 citing papers in PubMed, 57 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Review
  10. Overview of Oxidative Stress in Systemic Lupus Erythematosus.Antioxidants (Basel, Switzerland) · 2025
    Review
  11. Article
  12. Article
  13. Towards precision medicine for systemic lupus erythematosus and neuropsychiatric manifestations.Expert review of precision medicine and drug development · 2025
    Article
  14. Review
  15. Review
  16. Review
  17. Observational
  18. Annals of the rheumatic diseases · 2024
    Article
  19. Article
  20. Article
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

2 authors at 2 institutions in 1 country.

Isaac T W HarleyDivision of Rheumatology, Department of Medicine, University of Colorado School of Medicine, Aurora, CO, USA; Human Immunology and Immunotherapy Initiative (HI(3)), Department of Immunology, University of Colorado School of Medicine, Aurora, CO, USA; Rocky Mountain Regional Veteran's Administration Medical Center (VAMC), Medicine Service, Rheumatology Section, Aurora, CO, USA. Electronic address: ISAAC.HARLEY@CUANSCHUTZ.EDU.
Amr H SawalhaDivision of Rheumatology, Department of Pediatrics, University of Pittsburgh School of Medicine, UPMC Children's Hospital of Pittsburgh, Pittsburgh, PA, USA; Division of Rheumatology and Clinical Immunology, Department of Medicine, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA; Department of Immunology, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA; Lupus Center of Excellence, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA. Electronic address: asawalha@pitt.edu.
Rocky Mountain MS Center · USUniversity of Pittsburgh · US

Funding

Role of DNA methylation in lupusR01AI097134 · NIAID · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI Amr H Sawalha · 2013 to 2026
$4.5M
Characterizing the Takayasu Arteritis Genetic Risk in RPS9/LILRB3R01AR070148 · NIAMS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI SAWALHA, AMR H · 2017 to 2022
$1.7M
NIAID NIH HHS R01 AI097134NIAMS NIH HHS R01 AR070148
6 · The paper itself

Abstract

Systemic lupus erythematosus is the prototypical systemic autoimmune disease, as it is characterized both by protean multi-organ system manifestations and by the uniform presence of pathogenic autoantibodies directed against components of the nucleus. Prior to the modern genetic era, the diverse clinical manifestations of SLE suggested to many that SLE patients were unlikely to share a common genetic risk basis. However, modern genetic studies have revealed that SLE usually arises when an environmental exposure occurs in an individual with a collection of genetic risk variants passing a liability threshold. Here, we summarize the current state of the field aimed at: (1) understanding the genetic architecture of this complex disease, (2) synthesizing how this genetic risk architecture impacts cellular and molecular disease pathophysiology, (3) providing illustrative examples that highlight the rich complexity of the pathobiology of this prototypical autoimmune disease and (4) communicating this complex etiopathogenesis to patients.

Indexed as

Autoimmune DiseasesLupus Erythematosus, SystemicAutoantibodiesHumansRisk FactorsAutoantibodies

Identifiers

PMID35149194
PMCPMC9167620
OpenAlexW4210890207

What OpenQuestion holds

Textmetadata
LicenceTDM
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.