Evidence map›Paper›PMID 17963047›Full record

ReviewClinical reviews in allergy & immunology2007

Horizons in Sjögren's syndrome genetics.

Pamela H Williams, Beth L Cobb, Bahram Namjou, R Hal Scofield, Amr H Sawalha, John B Harley

Abstract readReview
In one paragraph

Review in Clinical reviews in allergy & immunology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed, 1 pooled it
1.2field-weighted citation impact, top 22% 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

8 citing papers in PubMed, 1 synthesis or guideline pooled it, 16 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Vasculitis: current status and future directions.Clinical reviews in allergy & immunology · 2008
    Article
  8. Cutting edge issues in autoimmunity.Clinical reviews in allergy & immunology · 2008
    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

6 authors at 3 institutions in 1 country.

Pamela H WilliamsArthritis and Immunology Program, Oklahoma Medical Research Foundation, Oklahoma City 73104, USA.
Beth L Cobb
Bahram Namjou
R Hal Scofield
Amr H Sawalha
John B Harley
Oklahoma Medical Research Foundation · USUnited States Department of Veterans Affairs · USUniversity of Oklahoma Health Sciences Center · US

Funding

THE EFFECTS OF ERK PATHWAY INHIBITION ON DNA METHYLATION IN SLEP20RR015577 · NCRR · OKLAHOMA MEDICAL RESEARCH FOUNDATION · PI CENTOLA, MICHAEL B · 2000 to 2009
$21.5M
VALIDATING NOVEL GENES IMPLICATED IN LEUKOCYTE CHEMOTAXISP20RR020143 · NCRR · OKLAHOMA MEDICAL RESEARCH FOUNDATION · PI GAFFNEY, PATRICK M · 2004 to 2011
$21.0M
Program Project in the Genetics of SLEP01AR049084 · NIAMS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI HARLEY, JOHN BARKER · 2002 to 2012
$12.7M
HLA GENE COMPLEMENTATION IN PRIMARY SJOGREN'S AND LUPUSR01AI024717 · NIAID · OKLAHOMA MEDICAL RESEARCH FOUNDATION · PI KOTTYAN, LEAH CLAIRE, WEIRAUCH, MATTHEW TYSON · 1987 to 2025
$7.8M
SNP Confirmation and High Throughput Genotyping CoreP30AR053483 · NIAMS · OKLAHOMA MEDICAL RESEARCH FOUNDATION · PI GUTHRIDGE, JOEL MARVIN · 2007 to 2017
$6.7M
THROMBOCYTOPENIA AND THE GENETICS OF SEVERE LUPUSP50AR048940 · NIAMS · OKLAHOMA MEDICAL RESEARCH FOUNDATION · PI REICHLIN, MORRIS · 2002 to 2006
$5.8M
GENETIC ASSOCIATION WITH LUPUS IN AMERICAN BLACKSR01AR042460 · NIAMS · OKLAHOMA MEDICAL RESEARCH FOUNDATION · PI HARLEY, JOHN BARKER · 1993 to 2009
$5.1M
Genetic Linkage in LupusR37AI024717 · NIAID · OKLAHOMA MEDICAL RESEARCH FOUNDATION · PI HARLEY, JOHN BARKER · 2005 to 2014
$4.2M
Y RNA SEQUENCES AND RO RNP FUNCTIONR01AI031584 · NIAID · OKLAHOMA MEDICAL RESEARCH FOUNDATION · PI HARLEY, JOHN BARKER · 1991 to 2006
$2.7M
Genetic Association in Sjogren's SyndromeR01DE015223 · NIDCR · OKLAHOMA MEDICAL RESEARCH FOUNDATION · PI HARLEY, JOHN BARKER · 2004 to 2008
$1.9M
LUPUS MULTIPLEX REGISTRY AND REPOSITORY-264012253N01AR012253 · NIAMS · OKLAHOMA MEDICAL RESEARCH FDN · 2002 to 2005
–
NCRR NIH HHS P20 RR015577NCRR NIH HHS P20-RR015577NCRR NIH HHS P20 RR020143NCRR NIH HHS RR020143NIAID NIH HHS AI24717NIAID NIH HHS AI31584NIAID NIH HHS R01 AI024717NIAID NIH HHS R01 AI031584NIAID NIH HHS R37 AI024717NIAMS NIH HHS AR048940NIAMS NIH HHS AR049084NIAMS NIH HHS AR42460NIAMS NIH HHS N01 AR012253NIAMS NIH HHS P01 AR049084NIAMS NIH HHS P30 AR053483NIAMS NIH HHS P50 AR048940NIAMS NIH HHS R01 AR042460NIDCR NIH HHS DE015223NIDCR NIH HHS R01 DE015223
6 · The paper itself

Abstract

Sjögren's syndrome (SS) is a complex polygenic autoimmune disorder. A few major genetic effects have been identified. Historically, HLA and non-HLA genetic associations have been reported. Recently, the HLA region continued to reveal association findings. A new susceptibility region has been suggested by a study of a D6S349 microsatellite marker. Among non-HLA studies, recent association of immunoglobulin kappa chain allotype KM1 with anti-La autoantibodies in primary Sjögren's syndrome confirms findings in a study from two decades ago. Meanwhile, mouse models have been employed to study the genetic contribution to salivary lymphadenitis or dry eyes and mouth. Gene transfer exploration in mouse models shows promise. The authors review the HLA and non-HLA association studies and the mouse model work that has been reported. Newly developed genomic capacity will provide, in the future, a much closer approximation of the true picture of the genetic architecture of Sjögren's syndrome.

Indexed as

Genetic Predisposition to DiseaseAnimalsDisease Models, AnimalHLA AntigensHumansMiceSjogren's SyndromeHLA Antigens

Identifiers

PMID17963047
PMCPMC4420170
OpenAlexW2011231618

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.