Evidence map›Paper›PMID 36577442›Full record

ArticleArthritis & rheumatology (Hoboken, N.J.)2023

Paradoxical Effects of Endoplasmic Reticulum Aminopeptidase 1 Deficiency on HLA-B27 and Its Role as an Epistatic Modifier in Experimental Spondyloarthritis.

Tri M Tran, Tejpal Gill, Joshua Bennett, Sohee Hong, Vance Holt, Anders J Lindstedt, Sufia Bakshi, Keith Sikora, Joel D Taurog, Maxime Breban and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in Arthritis & rheumatology (Hoboken, N.J.), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.6field-weighted citation impact, top 9% 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

14 citing papers in PubMed, 18 citations in OpenAlex.

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  10. Biology of HLA class I associated inflammatory diseases.Best practice & research. Clinical rheumatology · 2024
    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

12 authors at 3 institutions in 2 countries.

Tri M TranPediatric Translational Research Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, NIH, Bethesda, Maryland.
Tejpal GillPediatric Translational Research Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, NIH, Bethesda, Maryland.ORCID 0000-0002-9567-3827
Joshua BennettPediatric Translational Research Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, NIH, Bethesda, Maryland.
Sohee HongPediatric Translational Research Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, NIH, Bethesda, Maryland.
Vance HoltPediatric Translational Research Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, NIH, Bethesda, Maryland.
Anders J LindstedtPediatric Translational Research Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, NIH, Bethesda, Maryland.
Sufia BakshiPediatric Translational Research Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, NIH, Bethesda, Maryland.
Keith SikoraPediatric Translational Research Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, NIH, Bethesda, Maryland.
Joel D TaurogDivision of Rheumatic Diseases, Department of Medicine, University of Texas Southwestern Medical Center, Dallas.
Maxime BrebanInfection and Inflammation Department, UMR1173, INSERM, Université de Versailles Saint-Quentin-en-Yvelines/Université Paris Saclay, and Rheumatology Department, Ambroise Paré Hospital, Paris, France.
Fatemeh NavidPediatric Translational Research Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, NIH, Bethesda, Maryland.
Robert A ColbertPediatric Translational Research Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, NIH, Bethesda, Maryland.ORCID 0000-0001-6237-4575
National Institute of Arthritis and Musculoskeletal and Skin Diseases · USInserm · FRThe University of Texas Southwestern Medical Center · US

Funding

Pathogenic Mechanisms in SpondyloarthritisZIAAR041184 · NIAMS · NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES · PI COLBERT, ROBERT · 2009 to 2025
$47.6M
Intramural NIH HHS ZIA AR041184
6 · The paper itself

Abstract

objectiveWe undertook this study to examine the functional basis for epistasis between endoplasmic reticulum aminopeptidase 1 (ERAP1) and HLA-B27 in experimental spondyloarthritis (SpA).

methodsERAP1-knockout rats were created using genome editing and bred with HLA-B27/human β

resultsERAP1 deficiency increased the ratio of folded to unfolded (β

conclusionERAP1 deficiency reduced HLA-B27 misfolding and improved folding while having opposing effects on HLA-B7. The finding that HLA-B27-Tg rats had partial protection against SpA in this study is consistent with genetic evidence that loss-of-function and/or reduced expression of ERAP1 reduces the risk of ankylosing spondylitis. Functional studies support the concept that the effects of ERAP1 on HLA-B27 and SpA may be a consequence of how peptides affect the biology of this allotype rather than their role as antigenic determinants.

Indexed as

HLA-B27 AntigenSpondylitis, AnkylosingAminopeptidasesAnimalsArthritisEndoplasmic ReticulumHLA-B7 AntigenHumansMinor Histocompatibility AntigensRatsAminopeptidasesERAP1 protein, humanHLA-B27 AntigenHLA-B7 AntigenMinor Histocompatibility Antigens

Identifiers

PMID36577442
PMCPMC9892207
OpenAlexW4291798751

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.