Evidence map›Paper›PMID 20193000›Full record

ReviewImmunological reviews2010

From HLA-B27 to spondyloarthritis: a journey through the ER.

Robert A Colbert, Monica L DeLay, Erin I Klenk, Gerlinde Layh-Schmitt

Open access · greenAbstract readReview
In one paragraph

Review in Immunological reviews, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers.

0numbers the graph read from it
0cells of the map it votes in
84citing papers in PubMed
4.9field-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

84 citing papers in PubMed, 177 citations in OpenAlex.

  1. Trial
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  12. The Role of Aminopeptidase ERAP1 in Human Pathology-A Review.Current issues in molecular biology · 2024
    Review
  13. Article
  14. Article
  15. Journal of immunology research · 2022
    Article
  16. Article
  17. Review
  18. Review
  19. Article
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24 more citing papers are in PubMed but not listed here.

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

4 authors at 2 institutions in 1 country.

Robert A ColbertNational Institute of Arthritis and Musculoskeletal and Skin Diseases, NIH, Bethesda, MD 20892, USA. colbertr@mail.nih.gov
Monica L DeLay
Erin I Klenk
Gerlinde Layh-Schmitt
Cincinnati Children's Hospital Medical Center · USNational Institute of Arthritis and Musculoskeletal and Skin Diseases · US

Funding

Pathogenic Mechanisms in SpondyloarthritisZIAAR041184 · NIAMS · NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES · PI COLBERT, ROBERT · 2009 to 2025
$47.6M
MECHANISM AND CONSEQUENCES OF HLA-B 27 MISFOLDINGR01AR046177 · NIAMS · CINCINNATI CHILDRENS HOSP MED CTR · PI GRIFFIN, THOMAS A · 2000 to 2010
$3.0M
HLA-B27 Misfolding in Spondyloarthropathy PathogenesisR01AR048372 · NIAMS · CHILDREN'S HOSPITAL MED CTR (CINCINNATI) · PI COLBERT, ROBERT A. · 2001 to 2005
$1.8M
Intramural NIH HHS Z99 AR999999NIAMS NIH HHS AR46177NIAMS NIH HHS AR48372NIAMS NIH HHS R01 AR046177NIAMS NIH HHS R01 AR048372
6 · The paper itself

Abstract

Almost four decades of research into the role of human leukocyte antigen-B27 (HLA-B27) in susceptibility to spondyloarthritis has yet to yield a convincing answer. New results from an HLA-B27 transgenic rat model now demonstrate quite convincingly that CD8(+) T cells are not required for the inflammatory phenotype. Discoveries that the HLA-B27 heavy chain has a tendency to misfold during the assembly of class I complexes in the endoplasmic reticulum (ER) and to form aberrant disulfide-linked dimers after transport to the cell surface have forced the generation of new ideas about its role in disease pathogenesis. In transgenic rats, HLA-B27 misfolding generates ER stress and leads to activation of the unfolded protein response, which dramatically enhances the production of interleukin-23 (IL-23) in response to pattern recognition receptor agonists. These findings have led to the discovery of striking T-helper 17 cell activation and expansion in this animal model, consistent with results emerging from humans with spondyloarthritis and the discovery of IL23R as an additional susceptibility gene for ankylosing spondylitis. Together, these results suggest a novel link between HLA-B27 and the T-helper 17 axis through the consequences of protein misfolding and open new avenues of investigation as well as identifying new targets for therapeutic intervention in this group of diseases.

Indexed as

AnimalsDisease Models, AnimalEndoplasmic ReticulumGenetic Predisposition to DiseaseHLA-B27 AntigenHumansInterleukin-23MiceMice, TransgenicProtein FoldingProtein MultimerizationProtein TransportRatsRats, TransgenicReceptors, InterleukinReceptors, Pattern RecognitionHLA-B27 AntigenIL23R protein, humanInterleukin-23Receptors, InterleukinReceptors, Pattern Recognition

Identifiers

PMID20193000
PMCPMC2912611
OpenAlexW1985192443

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.