Evidence map›Paper›PMID 17619875›Full record

ArticleImmunogenetics2007

Subcongenic analysis of genetic basis for impaired development of invariant NKT cells in NOD mice.

Yi-Guang Chen, John P Driver, Pablo A Silveira, David V Serreze

Abstract read
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In one paragraph

Article in Immunogenetics, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

11 citing papers in PubMed, 23 citations in OpenAlex.

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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

4 authors at 2 institutions in 2 countries.

Yi-Guang ChenThe Jackson Laboratory, 600 Main Street, Bar Harbor, ME 04609, USA.
John P Driver
Pablo A Silveira
David V Serreze
Jackson Laboratory · USGarvan Institute of Medical Research · AU

Funding

Shared Resource ManagementP30CA034196 · NCI · JACKSON LABORATORY · PI William Carl Skarnes · 1985 to 2026
$61.9M
Diabetogenic Role of MHC Class I Alleles in NOD MiceR01DK046266 · NIDDK · JACKSON LABORATORY · PI SERREZE, DAVID V · 2000 to 2018
$7.2M
ANTIGEN PRESENTING CELL DEFECTS IN AUTOIMMUNE DIABETESR01DK051090 · NIDDK · JACKSON LABORATORY · PI SERREZE, DAVID V · 1996 to 2009
$3.0M
DIABETOGENIC ROLE OF H-2G7 CLASS I ALLELES IN NOD MICER29DK046266 · NIDDK · JACKSON LABORATORY · PI SERREZE, DAVID V. · 1993 to 1998
–
NCI NIH HHS CA34196NIDDK NIH HHS DK46266NIDDK NIH HHS DK51090
6 · The paper itself

Abstract

Reduced numbers and function of invariant NKT (iNKT) cells partially contribute to type 1 diabetes (T1D) development in NOD mice. Previous linkage analysis identified a genetic locus on chromosome 2 controlling numbers of thymic iNKT cells. Interestingly, this locus resides within the Idd13 region that distinguishes NOD mice from the closely genetically related, but strongly T1D-resistant NOR strain. Thus, we tested if a genetic variant that confers T1D resistance in NOR mice may do so by enhancing iNKT cell numbers. iNKT cells were enumerated by an alpha-GalCer analog loaded CD1d tetramer in NOD and NOR mice as well as in NOD stocks carrying NOR-derived congenic regions on chromosome 1, 2, or 4. Significantly, more thymic and splenic iNKT cells were present in NOR than NOD mice. The NOR-derived Idd13 region on chromosome 2 contributed the most significant effect on increasing iNKT cell numbers. Subcongenic analyses indicated that at least two genes within the Idd13 region regulate iNKT cell numbers. These results further define the genetic basis for numerical iNKT cell defects contributing to T1D development in NOD mice.

Indexed as

Genetic Predisposition to DiseaseAnimalsAntigens, CD1Diabetes Mellitus, Type 1Killer Cells, NaturalLymphocyte ActivationLymphocyte CountMiceMice, CongenicMice, Inbred NODSpecies SpecificityAntigens, CD1

Identifiers

PMID17619875
OpenAlexW1995784968

What OpenQuestion holds

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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.