Evidence map›Paper›PMID 23727634›Full record

ArticleAnnals of the rheumatic diseases2014

MICA, a gene contributing strong susceptibility to ankylosing spondylitis.

Xiaodong Zhou, Jiucun Wang, Hejian Zou, Michael M Ward, Michael H Weisman, Maribel G Espitia, Xiangjun Xiao, Effie Petersdorf, Emmanuel Mignot, Javier Martin and 3 more

Open access · greenAbstract read
In one paragraph

Article in Annals of the rheumatic diseases, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed, 3 pooled it
1.8field-weighted citation impact, top 15% 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

36 citing papers in PubMed, 3 syntheses or guidelines pooled it, 54 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
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  4. Trial
  5. Review
  6. Review
  7. Article
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  12. Article
  13. Article
  14. High population frequencies ofFrontiers in immunology · 2023
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  16. Journal of personalized medicine · 2021
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  17. Association of ProtectiveFrontiers in genetics · 2021
    Article
  18. Leveraging NKG2D Ligands in Immuno-Oncology.Frontiers in immunology · 2021
    Review
  19. Review
  20. Frontiers in genetics · 2020
    Article
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

13 authors at 9 institutions in 3 countries.

Xiaodong ZhouDepartment of Internal Medicine, Division of Rheumatology, The University of Texas Medical School at Houston, Houston, Texas, USA.
Jiucun WangMinistry of Education (MOE) Key Laboratory of Contemporary Anthropology, School of Life Sciences, Fudan University, Shanghai, China.
Hejian ZouDepartment of Rheumatology, Huashan Hospital, Fudan University, Shanghai, China.
Michael M WardNIAMS, Bethesda, Maryland, USA.
Michael H WeismanDepartment of Medicine, Cedars-Sinai Medical Center, Los Angeles, California, USA.
Maribel G EspitiaDepartment of Internal Medicine, Division of Rheumatology, The University of Texas Medical School at Houston, Houston, Texas, USA.
Xiangjun XiaoDepartment of Epidemiology, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.
Effie PetersdorfDivision of Clinical Research, Fred Hutchinson Cancer Research Center, Department of Medicine and Division of Oncology, University of Washington, Seattle, Washington, USA.
Emmanuel MignotDepartment of Psychiatry, Stanford University, School of Medicine, Stanford, California, USA.
Javier MartinThe Instituto de Parasitologia y Biomedicina Lopez-Neyra, CSIC, Armilla, Granada, Spain.
Lianne S GenslerDivision of Rheumatology, The University of California, San Francisco, USA.
Paul ScheetDepartment of Epidemiology, The University of Texas MD Anderson Cancer Center, Houston, Texas, USA.
John D ReveilleDepartment of Internal Medicine, Division of Rheumatology, The University of Texas Medical School at Houston, Houston, Texas, USA.
The University of Texas MD Anderson Cancer Center · USCedars-Sinai Medical Center · USFudan University · CNHuashan Hospital · CNInstituto de Parasitología y Biomedicina "López - Neyra" · ESNational Institute of Arthritis and Musculoskeletal and Skin Diseases · USStanford University · USUniversity of California, San Francisco · USUniversity of Washington · US

Funding

Clinical Support Services for the NIAMS Intramural Research ProgramZIDAR041180 · NIAMS · NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES · PI COLBERT, ROBERT · 2009 to 2025
$119.2M
Center for Clinical and Translational Sciences (CCTS)UL1TR000371 · NCATS · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI MCPHERSON, DAVID D · 2012 to 2016
$13.4M
Outcomes in Rheumatic DiseasesZIAAR041153 · NIAMS · NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES · PI WARD, MICHAEL · 2009 to 2020
$12.6M
The Genetic Basis of AS SusceptibilityP01AR052915 · NIAMS · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI BROWN, MATTHEW A · 2006 to 2016
$10.9M
Studies of HLA Region Genomics in Systemic Sclerosis and Ankylosing SpondyilitisU01AI090909 · NIAID · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI MAYES, MAUREEN MAUREEN, REVEILLE, JOHN DUFFIN · 2010 to 2014
$2.9M
NCATS NIH HHS UL1 TR000371NIAID NIH HHS 1U01AI09090-01NIAID NIH HHS U01 AI090909NIAMS NIH HHS P01 AR052915PHS HHS P01-052915-01
6 · The paper itself

Abstract

objectiveThe human major histocompatibility complex class I chain-related gene A (MICA) controls the immune process by balancing activities of  natural killer cells, γδ T cells and αβ CD8 T cells, and immunosuppressive CD4 T cells. MICA is located near HLA-B on chromosome 6. Recent genomewide association studies indicate that genes most strongly linked to ankylosing spondylitis (AS) susceptibility come from the region containing HLA-B and MICA. While HLA-B27 is a well-known risk genetic marker for AS, the potential effect of linkage disequilibrium (LD) shields any associations of genes around HLA-B with AS. The aim of this study was to investigate a novel independent genetic association of MICA to AS.

methodsWe examined 1543 AS patients and 1539 controls from two ethnic populations by sequencing MICA and genotyping HLA-B alleles. Initially, 1070 AS patients and 1003 controls of European ancestry were used as a discovery cohort, followed by a confirmation cohort of 473 Han Chinese AS patients and 536 controls. We performed a stratified analysis based on HLA-B27 carrier status. We also conducted logistic regression with a formal interaction term.

resultsSequencing of MICA identified that MICA*007:01 is a significant risk allele for AS in both Caucasian and Han Chinese populations, and that MICA*019 is a major risk allele in Chinese AS patients. Conditional analysis of MICA alleles on HLA-B27 that unshielded LD effect confirmed associations of the MICA alleles with AS.

conclusionsParallel with HLA-B27, MICA confers strong susceptibility to AS in US white and Han Chinese populations.

Indexed as

AdultAsianCohort StudiesFemaleGenetic MarkersGenetic Predisposition to DiseaseHistocompatibility Antigens Class IHLA-B AntigensHumansLinkage DisequilibriumMaleMiddle AgedRisk FactorsSpondylitis, AnkylosingUnited StatesWhite PeopleGenetic MarkersHistocompatibility Antigens Class IHLA-B AntigensMHC class I-related chain AAnkylosing SpondylitisGene PolymorphismInflammation

Identifiers

PMID23727634
PMCPMC3874076
OpenAlexW2169289693

What OpenQuestion holds

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Registered trials

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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.