Evidence map›Paper›PMID 37957180›Full record

ArticleScientific reports2023

Human leukocyte antigen-DQ risk heterodimeric haplotypes of left ventricular dysfunction in cardiac sarcoidosis: an autoimmune view of its role.

Hironori Yamamoto, Yohei Miyashita, Hitoshi Minamiguchi, Kazuyoshi Hosomichi, Shohei Yoshida, Hidetaka Kioka, Haruki Shinomiya, Haruno Nagata, Kenji Onoue, Masato Kawasaki and 12 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.7field-weighted citation impact, top 29% 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

3 citing papers in PubMed, 4 citations in OpenAlex.

  1. Article
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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

22 authors at 9 institutions in 1 country.

Hironori YamamotoDepartment of Cardiovascular Medicine, Osaka University Graduate School of Medicine, 2-2 Yamadaoka, Suita, Osaka, 565-0871, Japan.
Yohei MiyashitaDepartment of Cardiovascular Medicine, Osaka University Graduate School of Medicine, 2-2 Yamadaoka, Suita, Osaka, 565-0871, Japan. miyashita.yohei@ncvc.go.jp.
Hitoshi MinamiguchiDepartment of Cardiovascular Medicine, Osaka University Graduate School of Medicine, 2-2 Yamadaoka, Suita, Osaka, 565-0871, Japan.
Kazuyoshi HosomichiLaboratory of Computational Genomics, School of Life Science, Tokyo University of Pharmacy and Life Sciences, Hachioji, Tokyo, 192-0392, Japan.
Shohei YoshidaDepartment of Cardiovascular Medicine, Kanazawa University Hospital, Kanazawa, Ishikawa, 920-8641, Japan.
Hidetaka KiokaDepartment of Cardiovascular Medicine, Osaka University Graduate School of Medicine, 2-2 Yamadaoka, Suita, Osaka, 565-0871, Japan.
Haruki ShinomiyaDepartment of Cardiovascular Medicine, Osaka University Graduate School of Medicine, 2-2 Yamadaoka, Suita, Osaka, 565-0871, Japan.
Haruno NagataDepartment of Cardiovascular Medicine, University of the Ryukyus Graduate School of Medicine, Nakagami, Okinawa, 903-0215, Japan.
Kenji OnoueDepartment of Cardiovascular Medicine, Nara Medical University, Kashihara, Nara, 634-8522, Japan.
Masato KawasakiDepartment of Cardiology, Osaka General Medical Center, Osaka, Osaka, 558-8558, Japan.
Yuki KuramotoDepartment of Cardiovascular Medicine, Osaka University Graduate School of Medicine, 2-2 Yamadaoka, Suita, Osaka, 565-0871, Japan.
Akihiro NomuraInnovative Research Center, Kanazawa University School of Medicine, Kanazawa, Ishikawa, 920-8641, Japan.
Yuichiro TomaDepartment of Cardiovascular Medicine, University of the Ryukyus Graduate School of Medicine, Nakagami, Okinawa, 903-0215, Japan.
Tetsuya WatanabeDepartment of Cardiology, Osaka General Medical Center, Osaka, Osaka, 558-8558, Japan.
Takahisa YamadaDepartment of Cardiology, Osaka General Medical Center, Osaka, Osaka, 558-8558, Japan.
Yasuki IshiharaDepartment of Cardiovascular Medicine, Osaka University Graduate School of Medicine, 2-2 Yamadaoka, Suita, Osaka, 565-0871, Japan.
Miho NagataDepartment of Cardiovascular Medicine, Osaka University Graduate School of Medicine, 2-2 Yamadaoka, Suita, Osaka, 565-0871, Japan.
Hisakazu KatoDepartment of Medical Biochemistry, Osaka University Graduate School of Medicine, Suita, Osaka, 565-0871, Japan.
Hideyuki HakuiDepartment of Cardiovascular Medicine, Osaka University Graduate School of Medicine, 2-2 Yamadaoka, Suita, Osaka, 565-0871, Japan.
Yoshihiko SaitoDepartment of Cardiovascular Medicine, Nara Prefecture Seiwa Medical Center, Nara, Nara, 636-0802, Japan.
Yoshihiro AsanoDepartment of Cardiovascular Medicine, Osaka University Graduate School of Medicine, 2-2 Yamadaoka, Suita, Osaka, 565-0871, Japan. asano.yoshihiro@ncvc.go.jp.
Yasushi SakataDepartment of Cardiovascular Medicine, Osaka University Graduate School of Medicine, 2-2 Yamadaoka, Suita, Osaka, 565-0871, Japan.
Osaka University · JPNara Medical University · JPOsaka Prefectural Medical Center · JPUniversity of the Ryukyus · JPKanazawa University · JPKanazawa University Hospital · JPKyoto University · JPOsaka City General Hospital · JPTokyo University of Pharmacy and Life Sciences · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cardiac sarcoidosis (CS) is the scarring of heart muscles by autoimmunity, leading to heart abnormalities and patients with sarcoidosis with cardiac involvements have poor prognoses. Due to the small number of patients, it is difficult to stratify all patients of CS by human leukocyte antigen (HLA) analysis. We focused on the structure of antigen-recognizing pockets in heterodimeric HLA-class II, in addition to DNA sequences, and extracted high-affinity combinations of antigenic epitopes from candidate autoantigen proteins and HLA. Four HLA heterodimer-haplotypes (DQA1*05:03/05:05/05:06/05:08-DQB1*03:01) were identified in 10 of 68 cases. Nine of the 10 patients had low left ventricular ejection fraction (< 50%). Fourteen amino-acid sequences constituting four HLA anchor pockets encoded by the HLA haplotypes were all common, suggesting DQA1*05:0X-DQB1*03:01 exhibit one group of heterodimeric haplotypes. The heterodimeric haplotypes recognized eight epitopes from different proteins. Assuming that autoimmune mechanisms might be activated by molecular mimicry, we searched for bacterial species having peptide sequences homologous to the eight epitopes. Within the peptide epitopes form the SLC25A4 and DSG2, high-homology sequences were found in Cutibacterium acnes and Mycobacterium tuberculosis, respectively. In this study, we detected the risk heterodimeric haplotypes of ventricular dysfunction in CS by searching for high-affinity HLA-class II and antigenic epitopes from candidate cardiac proteins.

Indexed as

SarcoidosisVentricular Dysfunction, LeftAllelesEpitopesGene FrequencyGenetic Predisposition to DiseaseHaplotypesHistocompatibility Antigens Class IHLA-DQ alpha-ChainsHLA-DQ AntigensHLA-DQ beta-ChainsHLA-DRB1 ChainsHumansPeptidesStroke VolumeVentricular Function, LeftEpitopesHistocompatibility Antigens Class IHLA-DQ alpha-ChainsHLA-DQ AntigensHLA-DQ beta-ChainsHLA-DRB1 ChainsPeptides

Identifiers

PMID37957180
PMCPMC10643531
OpenAlexW4388629952

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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.