Evidence map›Paper›PMID 25903069›Full record

ReviewJournal of human genetics2015

Human leukocyte antigen polymorphisms and personalized medicine for rheumatoid arthritis.

Hiroshi Furukawa, Shomi Oka, Kota Shimada, Atsushi Hashimoto, Shigeto Tohma

Open access · bronzeAbstract readReview
PubMed Publisher
In one paragraph

Review in Journal of human genetics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
4.5field-weighted citation impact, top 6% 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

20 citing papers in PubMed, 41 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Frontiers in immunology · 2025
    Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Associations ofGenes · 2023
    Article
  10. Article
  11. Article
  12. Current research status of HLA in immune-related diseases.Immunity, inflammation and disease · 2021
    Review
  13. Lessons from precision medicine in rheumatology.Multiple sclerosis (Houndmills, Basingstoke, England) · 2020
    Review
  14. Human Leukocyte Antigen-Disease Associations in Rheumatoid Arthritis.Rheumatic diseases clinics of North America · 2017
    Review
  15. Article
  16. Review
  17. Review
  18. Article
  19. 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

5 authors at 1 institution in 1 country.

Hiroshi FurukawaClinical Research Center for Allergy and Rheumatology, Sagamihara Hospital, National Hospital Organization, Sagamihara, Japan.ORCID http://orcid.org/0000-0002-4022-0767
Shomi OkaClinical Research Center for Allergy and Rheumatology, Sagamihara Hospital, National Hospital Organization, Sagamihara, Japan.
Kota ShimadaDepartment of Rheumatology, Sagamihara Hospital, National Hospital Organization, Sagamihara, Japan.
Atsushi HashimotoDepartment of Rheumatology, Sagamihara Hospital, National Hospital Organization, Sagamihara, Japan.
Shigeto TohmaClinical Research Center for Allergy and Rheumatology, Sagamihara Hospital, National Hospital Organization, Sagamihara, Japan.
National Sagamihara Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Human leukocyte antigen (HLA) polymorphisms are the most important genetic risk factors for rheumatoid arthritis (RA), a chronic systemic inflammatory disease of unknown etiology. Certain HLA-DRB1 alleles, known as shared epitope (SE) alleles because they have the same amino-acid sequence at positions 70-74, are associated with susceptibility to RA. A gene dosage effect is present for RA-predisposing SE alleles, and protective alleles show epistasis. An important role of amino-acid polymorphisms at positions 11 and 13 of the HLA-DRβ chain was also reported recently. Rheumatoid factor and anticitrullinated peptide antibodies are present in many RA patients. Similar to extra-articular manifestations, the presence of these autoantibodies is also associated with certain DRB1 alleles. Different frequencies of RA risk alleles in different ethnicities explain the varying prevalence of RA in different populations and suggest genetic heterogeneity of RA with regard to phenotype and population subsets. Some drug-induced hypersensitivity reactions due to disease-modifying antirheumatic drugs are also associated with HLA alleles. Understanding the role of HLA as the most important genetic factor relevant to RA susceptibility may help in determining its pathogenesis and pave the way to personalized medicine.

Indexed as

Antirheumatic AgentsArthritis, RheumatoidDrug HypersensitivityGenetic Predisposition to DiseaseHLA AntigensHumansPolymorphism, GeneticPrecision MedicineAntirheumatic AgentsHLA Antigens

Identifiers

PMID25903069
OpenAlexW2057448394

What OpenQuestion 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 OpenQuestion graph.