Evidence map›Paper›PMID 22487796›Full record

ReviewNature reviews. Rheumatology2012

Genetics of spondyloarthritis--beyond the MHC.

John D Reveille

Abstract readComparative StudyReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Rheumatology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 92 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
92citing papers in PubMed, 2 pooled it
11.9field-weighted citation impact, top 1% 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

92 citing papers in PubMed, 2 syntheses or guidelines pooled it, 196 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
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  6. Article
  7. Observational
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  11. Review
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  16. Association between HLA-B*27:04 and genetic susceptibility to ankylosing spondylitis in Hunan Province.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2023
    Article
  17. Article
  18. Review
  19. Review
  20. Review

32 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

1 author at 1 institution in 1 country.

John D ReveilleThe University of Texas Health Science Center at Houston, MSB 5.270, 6431 Fannin, Houston, TX 77030, USA. john.d.reveille@uth.tmc.edu
The University of Texas Health Science Center at Houston · US

Funding

NIAID NIH HHS 1U01AI090909‑01PHS HHS P01‑052,915‑01
6 · The paper itself

Abstract

Ankylosing spondylitis (AS), psoriasis and inflammatory bowel disease (IBD) often coexist in the same patient and in their families. In AS, genes within the MHC region, in particular HLA-B27, account for nearly 25% of disease hereditability, with additional small contributions from genes outside of the MHC locus, including those involved in intracellular antigen processing (that is, ERAP1, which interacts with HLA-B27) and cytokine genes such as those involved in the IL-17-IL-23 pathway. Similar to AS, the strongest genetic signal of susceptibility to psoriasis and psoriatic arthritis also emanates from the MHC region (attributable mostly to HLA-C(*)06:02 although other genes have been implicated), and gene-gene interaction of HLA-C with ERAP1. The remaining hereditary load is from genes involved in cytokine production, specifically genes in the IL-17-IL-23 pathway, the NFκB pathway and the type 2 T-helper pathway. In IBD, similar genetic influences are operative. Indeed, genes important in the regulation of the IL-17-IL-23 pathway and, in Crohn's disease, genes important for autophagy (that is, NOD2 and ATG16L1 and IRGM) have a role in conferring susceptibility of individuals to these diseases. Thus, AS, psoriasis and IBD seem to share similar pathogenic mechanisms of aberrant intracellular antigen processing or elimination of intracellular bacteria and cytokine production, especially in the IL-17-IL-23 pathway.

Indexed as

Arthritis, PsoriaticCytokinesDisease ProgressionFemaleFollow-Up StudiesGene Expression RegulationGenes, MHC Class IGenetic Predisposition to DiseaseHLA-B27 AntigenHLA-C AntigensHumansInflammatory Bowel DiseasesInterleukin-17MalePsoriasisRisk AssessmentCytokinesHLA-B27 AntigenHLA-C AntigensInterleukin-17

Identifiers

PMID22487796
OpenAlexW1560818763

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.