Evidence map›Paper›PMID 28756073›Full record

ArticlePresse medicale (Paris, France : 1983)

The genetics of Takayasu arteritis.

Paul Renauer, Amr H Sawalha

Abstract read
In one paragraph

Article in Presse medicale (Paris, France : 1983). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
5.3field-weighted citation impact, top 4% 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

32 citing papers in PubMed, 65 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. New avenues in childhood vasculitis.Pediatric rheumatology online journal · 2025
    Review
  6. Review
  7. Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Review
  13. Review
  14. Review
  15. Review
  16. Large-vessel vasculitis.Nature reviews. Disease primers · 2022
    Review
  17. Article
  18. Article
  19. Application progress of multiple imaging modalities in Takayasu arteritis.The international journal of cardiovascular imaging · 2021
    Review
  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 1 institution in 1 country.

Paul RenauerUniversity of Michigan, department of internal medicine, division of rheumatology, Ann Arbor, MI, USA.
Amr H SawalhaUniversity of Michigan, department of internal medicine, division of rheumatology, Ann Arbor, MI, USA; University of Michigan, center for computational medicine and bioinformatics, Ann Arbor, MI, USA. Electronic address: asawalha@umich.edu.
University of Michigan–Ann Arbor · US

Funding

Characterizing the Takayasu Arteritis Genetic Risk in RPS9/LILRB3R01AR070148 · NIAMS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI SAWALHA, AMR H · 2017 to 2022
$1.7M
NIAMS NIH HHS R01 AR070148
6 · The paper itself

Abstract

Takayasu arteritis (TAK) is a rare systemic vasculitis that is characterized by granulomatous inflammation of the aorta and its major branches. The cellular and biochemical processes involved in the pathogenesis of TAK are beginning to be elucidated, and implicate both cell and antibody-mediated autoimmune mechanisms. In addition, the underlying etiology to TAK may be explained, at least in part, by a complex genetic contribution. The most well-recognized genetic susceptibility locus for the disease is the classical HLA allele, HLA-B*52, which has been confirmed in several ethnicities. The genetic susceptibility with HLA-B*52, as well as additional classical alleles and loci, implicate both HLA class I and class II involvement in TAK. Furthermore, genetic associations with genes encoding immune response regulators, pro-inflammatory cytokines and mediators of humoral immunity may directly relate to disease mechanisms. Non-HLA susceptibility loci that have been recently established for TAK with a genome-wide level of significance include FCGR2A/FCGR3A, IL12B, IL6, RPS9/LILRB3, and a locus on chromosome 21 near PSMG1. In this review, we present the complex genetic predisposition to TAK and discuss how recent findings identified potential targets in the pathogenesis and treatment of the disease.

Indexed as

AllelesAntigens, CDGenetic Predisposition to DiseaseHistocompatibility Antigens Class IHistocompatibility Antigens Class IIHumansInterleukin-12 Subunit p40Interleukin-6Receptors, IgGReceptors, ImmunologicTakayasu ArteritisAntigens, CDFCGR2A protein, humanHistocompatibility Antigens Class IHistocompatibility Antigens Class IIIL12B protein, humanInterleukin-12 Subunit p40Interleukin-6LILRB3 protein, humanReceptors, IgGReceptors, Immunologic

Identifiers

PMID28756073
PMCPMC5753771
OpenAlexW2737838304

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.