Evidence map›Paper›PMID 34164946›Full record

ArticleArthritis & rheumatology (Hoboken, N.J.)2022

Anti-Double-Stranded DNA Antibodies Recognize DNA Presented on HLA Class II Molecules of Systemic Lupus Erythematosus Risk Alleles.

Hideaki Tsuji, Koichiro Ohmura, Hui Jin, Ryota Naito, Noriko Arase, Masako Kohyama, Tadahiro Suenaga, Shuhei Sakakibara, Yuta Kochi, Yukinori Okada and 5 more

Abstract read
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In one paragraph

Article in Arthritis & rheumatology (Hoboken, N.J.), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.0field-weighted citation impact, top 26% 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

6 citing papers in PubMed, 12 citations in OpenAlex.

  1. Observational
  2. Neoself Antigens Presented on MHC Class II Molecules in Autoimmune Diseases.Advances in experimental medicine and biology · 2024
    Article
  3. An Emerging Role for Anti-DNA Antibodies in Systemic Lupus Erythematosus.International journal of molecular sciences · 2023
    Review
  4. Anti-β2-glycoprotein I/HLA-DR Antibody and Adverse Obstetric Outcomes.International journal of molecular sciences · 2023
    Article
  5. Article
  6. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

15 authors at 6 institutions in 1 country.

Hideaki TsujiKyoto University, Kyoto, Japan; World Premier International Immunology Frontier Research Center, Osaka University, Suita, Japan, and Research Institute for Microbial Diseases, Osaka University, Suita, Japan.ORCID 0000-0002-2521-246X
Koichiro OhmuraKyoto University, Kyoto, Japan (current address: Kobe City Medical Center General Hospital, Kobe, Japan), : Kyoto University, Kyoto, Japan.
Hui JinResearch Institute for Microbial Diseases, Osaka University, Suita, Japan.
Ryota NaitoKyoto University, Kyoto, Japan; World Premier International Immunology Frontier Research Center, Osaka University, Suita, Japan, and Research Institute for Microbial Diseases, Osaka University, Suita, Japan.
Noriko AraseOsaka University Graduate School of Medicine, Suita, Japan.ORCID 0000-0003-3966-3437
Masako KohyamaWorld Premier International Immunology Frontier Research Center, Osaka University, Suita, Japan, and Research Institute for Microbial Diseases, Osaka University, Suita, Japan.
Tadahiro SuenagaWorld Premier International Immunology Frontier Research Center, Osaka University, Suita, Japan, and Research Institute for Microbial Diseases, Osaka University, Suita, Japan.
Shuhei SakakibaraWorld Premier International Immunology Frontier Research Center, Osaka University, Suita, Japan.
Yuta KochiRIKEN Center for Integrative Medical Sciences, Yokohama, Japan, and Tokyo Medical and Dental University, Tokyo, Japan.
Yukinori OkadaWorld Premier International Immunology Frontier Research Center, Osaka University, Suita, Japan; Osaka University Graduate School of Medicine, Suita, Japan and RIKEN Center for Integrative Medical Sciences, Yokohama, Japan.ORCID 0000-0002-0311-8472
Kazuhiko YamamotoRIKEN Center for Integrative Medical Sciences, Yokohama, Japan.
Hitoshi KikutaniWorld Premier International Immunology Frontier Research Center, Osaka University, Suita, Japan.
Akio MorinobuKyoto University, Kyoto, Japan (current address: Kobe City Medical Center General Hospital, Kobe, Japan), : Kyoto University, Kyoto, Japan.
Tsuneyo MimoriKyoto University, Kyoto, Japan (current address: Kobe City Medical Center General Hospital, Kobe, Japan), : Kyoto University, Kyoto, Japan.
Hisashi AraseWorld Premier International Immunology Frontier Research Center, Osaka University, Suita, Japan; Research Institute for Microbial Diseases, Osaka University, Suita, Japan, and Center for Infectious Disease Education and Research, Osaka University, Suita, Japan.ORCID 0000-0002-1153-3166
Kyoto University · JPOsaka International University · JPRIKEN Center for Integrative Medical Sciences · JPThe University of Osaka · JPJapan Research Institute · JPTokyo Medical and Dental University · JP

Funding

Japan Agency for Medical Research and Development JP20ek0410053JSPS KAKENHI JP18H05279JSPS KAKENHI JP18K19450MEXT KAKENHI JP190H04808
6 · The paper itself

Abstract

objectiveSpecific HLA class II alleles are associated with susceptibility to systemic lupus erythematosus (SLE). The role of HLA class II molecules in SLE pathogenesis remains unclear, although anti-DNA antibodies are specific to SLE and correlate with disease activity. We previously demonstrated that misfolded proteins bound to HLA class II molecules are specific targets for the autoantibodies produced in autoimmune diseases. This study was undertaken to validate our hypothesis that DNA binds to HLA class II molecules in a manner similar to that of misfolded proteins and that DNA bound to HLA class II molecules is involved in SLE pathogenesis.

methodsWe analyzed the binding of DNA to HLA class II molecules, as well as the response of cells expressing anti-DNA B cell receptors (BCRs) to cells expressing the DNA/HLA class II complex.

resultsEfficient binding of DNA to HLA class II molecules was observed in risk alleles of SLE, such as HLA-DRB1*15:01. The efficiency of DNA binding to each HLA-DR allele was positively associated with the risk of SLE conferred by the HLA-DR allele. In addition, reporter cells carrying anti-DNA BCRs were activated by cells expressing DNA/HLA class II complexes.

conclusionThese results provide evidence that DNA bound to HLA class II molecules is involved in SLE pathogenesis.

Indexed as

AllelesAntibodies, AntinuclearDNAHistocompatibility Antigens Class IIHumansLupus Erythematosus, SystemicRiskAntibodies, Antinuclearanti-dsDNA autoantibodyDNAHistocompatibility Antigens Class II

Identifiers

PMID34164946
OpenAlexW3173961337

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.