Evidence map›Paper›PMID 27796442›Full record

ArticleImmunogenetics2017

Congenic mapping identifies a novel Idd9 subregion regulating type 1 diabetes in NOD mice.

Bixuan Lin, Ashley E Ciecko, Erin MacKinney, David V Serreze, Yi-Guang Chen

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Immunogenetics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.6field-weighted citation impact, top 25% 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

1 citing paper in PubMed, 2 citations in OpenAlex.

  1. 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

5 authors at 2 institutions in 1 country.

Bixuan LinDepartment of Pediatrics, Max McGee National Research Center for Juvenile Diabetes, Medical College of Wisconsin, Milwaukee, WI, 53226, USA.
Ashley E CieckoDepartment of Pediatrics, Max McGee National Research Center for Juvenile Diabetes, Medical College of Wisconsin, Milwaukee, WI, 53226, USA.
Erin MacKinneyDepartment of Pediatrics, Max McGee National Research Center for Juvenile Diabetes, Medical College of Wisconsin, Milwaukee, WI, 53226, USA.
David V SerrezeThe Jackson Laboratory, Bar Harbor, ME, 04609, USA.
Yi-Guang ChenDepartment of Pediatrics, Max McGee National Research Center for Juvenile Diabetes, Medical College of Wisconsin, Milwaukee, WI, 53226, USA. yichen@mcw.edu.
Medical College of Wisconsin · USJackson Laboratory · US

Funding

Diabetogenic Role of MHC Class I Alleles in NOD MiceR01DK046266 · NIDDK · JACKSON LABORATORY · PI SERREZE, DAVID V · 2000 to 2018
$7.2M
B-lymphocyte Targeting Therapies for Autoimmune DiabetesR01DK095735 · NIDDK · JACKSON LABORATORY · PI SERREZE, DAVID V · 2013 to 2025
$6.2M
Mechanistic and Therapeutic Role of the CD137-CD137L Axis in Type 1 DiabetesR01DK107541 · NIDDK · MEDICAL COLLEGE OF WISCONSIN · PI CHEN, YI-GUANG, RIDGWAY, WILLIAM M · 2016 to 2025
$5.6M
Discovery and Functional Studies of Genes for T1D GWAS Susceptibility LociDP3DK097605 · NIDDK · MEDICAL COLLEGE OF WISCONSIN · PI CHEN, YI-GUANG, GEURTS, ARON M · 2012 to 2012
$4.3M
Role of the iNKT-Dendritic Cell Axis in Type 1 Diabetes in NOD MiceR00DK077443 · NIDDK · MEDICAL COLLEGE OF WISCONSIN · PI CHEN, YI-GUANG · 2010 to 2012
$736k
Genetic engineering of the Idd3 type 1 diabetes locusR21AI110963 · NIAID · MEDICAL COLLEGE OF WISCONSIN · PI CHEN, YI-GUANG · 2014 to 2015
$421k
A new genetic approach to identify the Idd9.3 type 1 diabetes susceptibility geneR21AI125879 · NIAID · MEDICAL COLLEGE OF WISCONSIN · PI CHEN, YI-GUANG · 2016 to 2017
$418k
Role of the iNKT-Dendritic Cell Axis in Type 1 Diabetes in NOD MiceK99DK077443 · NIDDK · JACKSON LABORATORY · PI CHEN, YI-GUANG · 2007 to 2009
$211k
DIABETOGENIC ROLE OF H-2G7 CLASS I ALLELES IN NOD MICER29DK046266 · NIDDK · JACKSON LABORATORY · PI SERREZE, DAVID V. · 1993 to 1998
–
NIAID NIH HHS R21 AI110963NIAID NIH HHS R21 AI125879NIDDK NIH HHS DP3 DK097605NIDDK NIH HHS K99 DK077443NIDDK NIH HHS R00 DK077443NIDDK NIH HHS R01 DK046266NIDDK NIH HHS R01 DK095735NIDDK NIH HHS R01 DK107541NIDDK NIH HHS R29 DK046266
6 · The paper itself

Abstract

Type 1 diabetes (T1D) results from complex interactions between genetic and environmental factors. The nonobese diabetic (NOD) mouse develops spontaneous T1D and has been used extensively to study the genetic control of this disease. T1D is suppressed in NOD mice congenic for the C57BL/10 (B10)-derived Idd9 resistance region on chromosome 4. Previous studies conducted by other investigators have identified four subregions (Idd9.1, Idd9.2, Idd9.3, and Idd9.4) where B10-derived genes suppress T1D development in NOD mice. We independently generated and characterized six congenic strains containing B10-derived intervals that partially overlap with the Idd9.1 and Idd9.4 regions. T1D incidence studies have revealed a new B10-derived resistance region proximal to Idd9.1. Our results also indicated that a B10-derived gene(s) within the Idd9.4 region suppressed the diabetogenic activity of CD4 T cells and promoted CD103 expression on regulatory T cells indicative of an activated phenotype. In addition, we suggest the presence of a B10-derived susceptibility gene(s) in the Idd9.1/Idd9.4 region. These results provide additional information to improve our understanding of the complex genetic control by the Idd9 region.

Indexed as

Genetic Predisposition to DiseaseAnimalsChromosome MappingDiabetes Mellitus, Type 1Genetic LociMiceMice, CongenicMice, Inbred C57BLMice, Inbred NODReceptors, Tumor Necrosis FactorT-Lymphocytes, RegulatoryReceptors, Tumor Necrosis FactorIdd9NOD mouseRegulatory T cellsType 1 diabetes

Identifiers

PMID27796442
PMCPMC5335865
OpenAlexW2544693968

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.