Evidence map›Paper›PMID 35749015›Full record

ReviewClinical reviews in allergy & immunology2023

A Summary on the Genetics of Systemic Lupus Erythematosus, Rheumatoid Arthritis, Systemic Sclerosis, and Sjögren's Syndrome.

Lourdes Ortíz-Fernández, Javier Martín, Marta E Alarcón-Riquelme

Abstract readReview
PubMed Publisher
In one paragraph

Review in Clinical reviews in allergy & immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed, 3 pooled it
8.2field-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

41 citing papers in PubMed, 3 syntheses or guidelines pooled it, 49 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Article
  5. A Versatile Anti-CXCR5 Monoclonal Antibody (CxCurrent issues in molecular biology · 2026
    Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. The Integrated Cellular and Molecular Landscape of Autoimmunity.bioRxiv : the preprint server for biology · 2025
    Article
  14. Article
  15. Review
  16. Review
  17. Zymography: Unveiling Matrix Metalloproteinase Dynamics.Methods in molecular biology (Clifton, N.J.) · 2025
    Article
  18. Frontiers in immunology · 2025
    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

3 authors at 2 institutions in 2 countries.

Lourdes Ortíz-FernándezInstitute of Parasitology and Biomedicine López-Neyra, CSIC, Parque Tecnológico de La Salud, 18016, Granada, Spain.
Javier MartínInstitute of Parasitology and Biomedicine López-Neyra, CSIC, Parque Tecnológico de La Salud, 18016, Granada, Spain.
Marta E Alarcón-RiquelmeGENYO. Center for Genomics and Oncological Research, Pfizer/University of Granada/Andalusian Regional Government, Av de la Ilustración 114, Parque Tecnológico de La Salud, 18016, Granada, Spain. marta.alarcon@genyo.es.ORCID http://orcid.org/0000-0002-7632-4154
Instituto de Parasitología y Biomedicina "López - Neyra" · ESKarolinska Institutet · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Systemic lupus erythematosus, systemic sclerosis, rheumatoid arthritis, and Sjögren's syndrome are four major autoimmune rheumatic diseases characterized by the presence of autoantibodies, caused by a dysregulation of the immune system that leads to a wide variety of clinical manifestations. These conditions present complex etiologies strongly influenced by multiple environmental and genetic factors. The human leukocyte antigen (HLA) region was the first locus identified to be associated and still represents the strongest susceptibility factor for each of these conditions, particularly the HLA class II genes, including DQA1, DQB1, and DRB1, but class I genes have also been associated. Over the last two decades, the genetic component of these disorders has been extensively investigated and hundreds of non-HLA risk genetic variants have been uncovered. Furthermore, it is widely accepted that autoimmune rheumatic diseases share molecular disease pathways, such as the interferon (IFN) type I pathways, which are reflected in a common genetic background. Some examples of well-known pleiotropic loci for autoimmune rheumatic diseases are the HLA region, DNASEL13, TNIP1, and IRF5, among others. The identification of the causal molecular mechanisms behind the genetic associations is still a challenge. However, recent advances have been achieved through mouse models and functional studies of the loci. Here, we provide an updated overview of the genetic architecture underlying these four autoimmune rheumatic diseases, with a special focus on the HLA region.

Indexed as

Arthritis, RheumatoidAutoimmune DiseasesLupus Erythematosus, SystemicRheumatic DiseasesScleroderma, SystemicSjogren's SyndromeAnimalsHistocompatibility Antigens Class IIHLA AntigensHumansInterferon Regulatory FactorsMiceHistocompatibility Antigens Class IIHLA AntigensInterferon Regulatory FactorsIrf5 protein, mouseAutoimmunityCommon variationGenome-wide association studyRheumatoid arthritisSystemic lupus erythematosusSystemic sclerosis

Identifiers

PMID35749015
OpenAlexW4283383583

What Socratic holds

Textmetadata
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 Socratic graph.