Evidence map›Paper›PMID 24498373›Full record

ArticlePloS one2014

Human leukocyte antigens and systemic lupus erythematosus: a protective role for the HLA-DR6 alleles DRB1*13:02 and *14:03.

Hiroshi Furukawa, Aya Kawasaki, Shomi Oka, Ikue Ito, Kota Shimada, Shoji Sugii, Atsushi Hashimoto, Akiko Komiya, Naoshi Fukui, Yuya Kondo and 22 more

Open access · goldAbstract readComparative Study
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 2 pooled it
5.1field-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

26 citing papers in PubMed, 2 syntheses or guidelines pooled it, 60 citations in OpenAlex.

  1. Pooled it
  2. Association ofChinese medical journal · 2018
    Pooled it
  3. Trial
  4. Review
  5. Article
  6. Article
  7. HLA Genetics for the Human Diseases.Advances in experimental medicine and biology · 2024
    Review
  8. HLA-DR genotypes in patients with systemic lupus erythematosus in Taiwan.Journal of the Chinese Medical Association : JCMA · 2023
    Article
  9. Article
  10. Genetic dissection ofRMD open · 2023
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
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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

32 authors at 13 institutions in 1 country.

Hiroshi FurukawaClinical Research Center for Allergy and Rheumatology, Sagamihara Hospital, National Hospital Organization, Sagamihara, Japan.
Aya KawasakiMolecular and Genetic Epidemiology Laboratory, Faculty of Medicine, University of Tsukuba, Tsukuba, Japan.
Shomi OkaClinical Research Center for Allergy and Rheumatology, Sagamihara Hospital, National Hospital Organization, Sagamihara, Japan.
Ikue ItoMolecular and Genetic Epidemiology Laboratory, Faculty of Medicine, University of Tsukuba, Tsukuba, Japan.
Kota ShimadaDepartment of Rheumatology, Tokyo Metropolitan Tama Medical Center, Fuchu, Japan ; Department of Rheumatology, Sagamihara Hospital, National Hospital Organization, Sagamihara, Japan.
Shoji SugiiDepartment of Rheumatology, Tokyo Metropolitan Tama Medical Center, Fuchu, Japan.
Atsushi HashimotoDepartment of Rheumatology, Sagamihara Hospital, National Hospital Organization, Sagamihara, Japan.
Akiko KomiyaClinical Research Center for Allergy and Rheumatology, Sagamihara Hospital, National Hospital Organization, Sagamihara, Japan.
Naoshi FukuiClinical Research Center for Allergy and Rheumatology, Sagamihara Hospital, National Hospital Organization, Sagamihara, Japan.
Yuya KondoDepartment of Internal Medicine, Faculty of Medicine, University of Tsukuba, Tsukuba, Japan.
Satoshi ItoDepartment of Rheumatology, Niigata Rheumatic Center, Shibata, Japan.
Taichi HayashiDepartment of Internal Medicine, Faculty of Medicine, University of Tsukuba, Tsukuba, Japan.
Isao MatsumotoDepartment of Internal Medicine, Faculty of Medicine, University of Tsukuba, Tsukuba, Japan.
Makio KusaoiDepartment of Internal Medicine and Rheumatology, Juntendo University School of Medicine, Tokyo, Japan.
Hirofumi AmanoDepartment of Internal Medicine and Rheumatology, Juntendo University School of Medicine, Tokyo, Japan.
Tatsuo NagaiDepartment of Rheumatology and Infectious Disease, Kitasato University School of Medicine, Sagamihara, Japan.
Shunsei HirohataDepartment of Rheumatology and Infectious Disease, Kitasato University School of Medicine, Sagamihara, Japan.
Keigo SetoguchiDepartment of Allergy and Immunological Diseases, Tokyo Metropolitan Cancer and Infectious Diseases Center Komagome Hospital, Tokyo, Japan.
Hajime KonoDepartment of Internal Medicine, Teikyo University, Tokyo, Japan.
Akira OkamotoDepartment of Rheumatology, Himeji Medical Center, National Hospital Organization, Himeji, Japan.
Noriyuki ChibaDepartment of Rheumatology, Morioka Hospital, National Hospital Organization, Morioka, Japan.
Eiichi SuematsuDepartment of Internal Medicine and Rheumatology, Clinical Research Institute, Kyushu Medical Center, National Hospital Organization, Fukuoka, Japan.
Masao KatayamaDepartment of Internal Medicine, Nagoya Medical Center, National Hospital Organization, Nagoya, Japan.
Kiyoshi MigitaClinical Research Center, Nagasaki Medical Center, National Hospital Organization, Omura, Japan.
Akiko SudaCenter for Rheumatic Diseases, Yokohama City University Medical Center, Yokohama, Japan ; Department of Rheumatology, Yokohama Minami Kyosai Hospital, Yokohama, Japan.
Shigeru OhnoCenter for Rheumatic Diseases, Yokohama City University Medical Center, Yokohama, Japan.
Hiroshi HashimotoJuntendo University School of Medicine, Tokyo, Japan.
Yoshinari TakasakiDepartment of Internal Medicine and Rheumatology, Juntendo University School of Medicine, Tokyo, Japan.
Takayuki SumidaDepartment of Internal Medicine, Faculty of Medicine, University of Tsukuba, Tsukuba, Japan.
Shouhei NagaokaDepartment of Rheumatology, Yokohama Minami Kyosai Hospital, Yokohama, Japan.
Naoyuki TsuchiyaMolecular and Genetic Epidemiology Laboratory, Faculty of Medicine, University of Tsukuba, Tsukuba, Japan.
Shigeto TohmaClinical Research Center for Allergy and Rheumatology, Sagamihara Hospital, National Hospital Organization, Sagamihara, Japan.
National Sagamihara Hospital · JPUniversity of Tsukuba · JPJuntendo University · JPKitasato University · JPNational Hospital Organization · JPYokohama Minami Kyosai Hospital · JPNagasaki Medical Center · JPNagoya Medical Center · JPNational Kyushu Medical Center · JPTeikyo University · JPTokyo Metropolitan Komagome Hospital · JPTokyo Metropolitan Tama Medical Center · JPYokohama City University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Many studies on associations between human leukocyte antigen (HLA) allele frequencies and susceptibility to systemic lupus erythematosus (SLE) have been performed. However, few protective associations with HLA-DRB1 alleles have been reported. Here, we sought protective, as well as predispositional, alleles of HLA-DRB1 in Japanese SLE patients. An association study was conducted for HLA-DRB1 in Japanese SLE patients. Relative predispositional effects were analyzed by sequential elimination of carriers of each allele with the strongest association. We also explored the association of DRB1 alleles with SLE phenotypes including the presence of autoantibody and clinical manifestations. Significantly different carrier frequencies of certain DRB1 alleles were found to be associated with SLE as follows: increased DRB1*15:01 (P = 5.48×10⁻¹⁰, corrected P (Pc) = 1.59×10⁻⁸, odds ratio [OR] 2.17, 95% confidence interval [CI] 1.69-2.79), decreased DRB1*13:02 (P = 7.17×10⁻⁵, Pc = 0.0020, OR 0.46, 95% CI 0.34-0.63) and decreased DRB1*14:03 (P = 0.0010, Pc = 0.0272, OR 0.34, 95% CI 0.18-0.63). Additionally, the "*15:01/*13:02 or *14:03" genotype tended to be negatively associated with SLE (P = 0.4209, OR 0.66), despite there being significant positive associations with *15:01 when present together with alleles other than *13:02 or *14:03 (P = 1.79×10⁻¹¹, OR 2.39, 95% CI 1.84-3.10). This protective effect of *13:02 and *14:03 was also confirmed in SLE patients with different clinical phenotypes. To the best of our knowledge, this is the first report of a protective association between the carrier frequencies of HLA-DRB1*13:02 and *14:03 and SLE in the Japanese population.

Indexed as

AdultAllelesAsian PeopleCase-Control StudiesDNAFemaleGenetic Predisposition to DiseaseGenotypeHLA-DR6 AntigenHLA-DRB1 ChainsHumansLupus Erythematosus, SystemicMaleMiddle AgedOdds RatioPolymerase Chain ReactionDNAHLA-DR6 AntigenHLA-DRB1 Chains

Identifiers

PMID24498373
PMCPMC3912000
OpenAlexW2059587387

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.