Evidence map›Paper›PMID 26324017›Full record

ReviewJournal of autoimmunity2015

Immunogenetics of systemic lupus erythematosus: A comprehensive review.

Yogita Ghodke-Puranik, Timothy B Niewold

Abstract readReview
In one paragraph

Review in Journal of autoimmunity, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 109 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
109citing papers in PubMed, 3 pooled it
18.8field-weighted citation impact, top 1% 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

109 citing papers in PubMed, 3 syntheses or guidelines pooled it, 224 citations in OpenAlex.

  1. Pooled it
  2. IL-33/IL-31 Axis in Immune-Mediated and Allergic Diseases.International journal of molecular sciences · 2019
    Pooled it
  3. Association ofChinese medical journal · 2018
    Pooled it
  4. Review
  5. Article
  6. Insulin-like growth factor receptor signaling in physiology and disease.Signal transduction and targeted therapy · 2026
    Review
  7. Review
  8. [Role of HLA genetic variants in autoimmune diseases].Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2026
    Review
  9. Review
  10. Review
  11. 3D Bioprinting Strategies in Autoimmune Disease Models.International journal of molecular sciences · 2025
    Review
  12. Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Review
  18. Review
  19. Review
  20. Article

49 more citing papers are in PubMed but not listed here.

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 1 institution in 1 country.

Yogita Ghodke-PuranikDivision of Rheumatology, Department of Immunology, Mayo Clinic, Rochester, MN, USA.
Timothy B NiewoldDivision of Rheumatology, Department of Immunology, Mayo Clinic, Rochester, MN, USA. Electronic address: Niewold.Timothy@mayo.edu.
Mayo Clinic in Arizona · US

Funding

Interferon Regulatory Factor 5 in Human Lupus PathogenesisR01AR065964 · NIAMS · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI NIEWOLD, TIMOTHY B · 2015 to 2018
$2.0M
Interferon Alpha as a Tool for Gene Discovery in Human LupusR01AR060861 · NIAMS · UNIVERSITY OF CHICAGO · PI NIEWOLD, TIMOTHY B · 2011 to 2015
$1.8M
The Role of IL-17 Axis in Inflammatory MyositisR01AR057781 · NIAMS · MAYO CLINIC ROCHESTER · PI NIEWOLD, TIMOTHY B, PETERSON, ERIK J · 2010 to 2014
$1.6M
NIAID NIH HHS AI071651NIAID NIH HHS L30 AI071651NIAMS NIH HHS AR057781NIAMS NIH HHS AR060861NIAMS NIH HHS AR065964NIAMS NIH HHS R01 AR057781NIAMS NIH HHS R01 AR060861NIAMS NIH HHS R01 AR065964
6 · The paper itself

Abstract

Our understanding of the genetic basis of systemic lupus erythematosus has progressed rapidly in recent years. While many genetic polymorphisms have been associated with disease susceptibility, the next major step involves integrating these genetic polymorphisms into the molecular mechanisms and cellular immunology of the human disease. In this review, we summarize some recent work in this area, including the genetics of the type I IFN response in SLE, including polygenic and monogenic factors, as well as epigenetic influences. Contributions of both HLA and non-HLA polymorphisms to the complex genetics of SLE are reviewed. We also review recent reports of specific gene deficits leading to monogenic SLE-like syndromes. The molecular functions of common SLE-risk variants are reviewed in depth, including regulatory variations in promoter and enhancer elements and coding-change polymorphisms, and studies which are beginning to define the molecular and cellular functions of these polymorphisms in the immune system. We discuss epigenetic influences on lupus, with an emphasis on micro-RNA expression and binding, as well as epigenetic modifications that regulate the expression levels of various genes involved in SLE pathogenesis and the ways epigenetic marks modify SLE susceptibility genes. The work summarized in this review provides a fascinating window into the biology and molecular mechanisms of human SLE. Understanding the functional mechanisms of causal genetic variants underlying the human disease greatly facilitates our ability to translate genetic associations toward personalized care, and may identify new therapeutic targets relevant to human SLE disease mechanisms.

Indexed as

Genetic Predisposition to DiseaseImmunogeneticsAnimalsAutoimmune DiseasesEpigenesis, GeneticGenetic LociHumansInterferon Type ILupus Erythematosus, SystemicMajor Histocompatibility ComplexMultifactorial InheritanceOpen Reading FramesPolymorphism, GeneticRegulatory Sequences, Nucleic AcidSignal TransductionInterferon Type IAutoimmune diseasesGeneticsInterferonSystemic lupus erythematosus

Identifiers

PMID26324017
PMCPMC4628859
OpenAlexW1538997551

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.