Evidence map›Paper›PMID 19032782›Full record

ArticleArthritis research & therapy2008

Identification of possible candidate genes regulating Sjögren's syndrome-associated autoimmunity: a potential role for TNFSF4 in autoimmune exocrinopathy.

Cuong Q Nguyen, Janet G Cornelius, Lauren Cooper, Jonathan Neff, Joann Tao, Byung Ha Lee, Ammon B Peck

Open access · goldAbstract readComparative Study
In one paragraph

Article in Arthritis research & therapy, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

22 citing papers in PubMed, 30 citations in OpenAlex.

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  16. Sjögren's syndrome: studying the disease in mice.Arthritis research & therapy · 2011
    Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 1 institution in 1 country.

Cuong Q NguyenDepartment of Oral Biology, University of Florida, Gainesville, FL 32610, USA. Nguyen@pathology.ufl.edu
Janet G Cornelius
Lauren Cooper
Jonathan Neff
Joann Tao
Byung Ha Lee
Ammon B Peck
University of Florida · US

Funding

NRSA Institutional Training Program in Oral BiologyT32DE007200 · NIDCR · UNIVERSITY OF FLORIDA · PI BURNE, ROBERT A · 1990 to 2010
$4.2M
Genetic Control of Autoimmune Exocrinopathy in NOD MiceR01DE014344 · NIDCR · UNIVERSITY OF FLORIDA · PI PECK, AMMON B · 2003 to 2007
$1.6M
NIDCR NIH HHS DE014344NIDCR NIH HHS R01 DE014344NIDCR NIH HHS T32 DE007200NIDCR NIH HHS T32DE07200
6 · The paper itself

Abstract

introductionSjögren syndrome (SjS) is a systemic autoimmune disease in which an immunological attack primarily against the salivary and lacrimal glands results in the loss of acinar cell tissue and function, leading to stomatitis sicca and keratoconjunctivitis sicca. In recent years, two genetic regions, one on chromosome 1 (designated autoimmune exocrinopathy 2 or Aec2) and the second on chromosome 3 (designated autoimmune exocrinopathy 1 or Aec1) derived from nonobese diabetic (NOD) mice, have been shown to be necessary and sufficient to replicate SjS-like disease in nonsusceptible C57BL/6 mice.

methodsStarting with the SjS-susceptible C57BL/6-derived mouse, referred to as C57BL/6.NOD-Aec1Aec2, we generated a large set of recombinant inbred (RI) lines containing portions of Aec2 as a means of identifying more precisely the genetic elements of chromosome 1 responsible for disease development.

resultsDisease profiling of these RI lines has revealed that the SjS susceptibility genes of Aec2 lie within a region located at approximately 79 +/- 5 cM distal to the centromere, as defined by microsatellite markers. This chromosomal region contains several sets of genes known to correlate with various immunopathological features of SjS as well as disease susceptibility genes for both type 1 diabetes and systemic lupus erythematosus in mice. One gene in particular, tumor necrosis factor (ligand) superfamily member 4 (or Ox40 ligand), encoding a product whose biological functions correlate with both physiological homeostasis and immune regulations, could be a potential candidate SjS susceptibility gene.

conclusionsThese new RI lines represent the first step not only in fine mapping SjS susceptibility loci but also in identifying potential candidate SjS susceptibility genes. Identification of possible candidate genes permits construction of models describing underlying molecular pathogenic mechanisms in this model of SjS and establishes a basis for construction of specific gene knockout mice.

Indexed as

AnimalsAntibodies, AntinuclearAutoimmune DiseasesCrosses, GeneticExocrine GlandsFemaleGenetic Predisposition to DiseaseMaleMembrane GlycoproteinsMiceMice, Inbred C57BLMice, Inbred NODOX40 LigandRecombination, GeneticSjogren's SyndromeTumor Necrosis FactorsAntibodies, AntinuclearMembrane GlycoproteinsOX40 LigandTnfsf4 protein, mouseTumor Necrosis Factors

Identifiers

PMID19032782
PMCPMC2656241
OpenAlexW2099137409

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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.