Evidence map›Paper›PMID 35760520›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2022

Nfkbid Overexpression in Nonobese Diabetic Mice Elicits Complete Type 1 Diabetes Resistance in Part Associated with Enhanced Thymic Deletion of Pathogenic CD8 T Cells and Increased Numbers and Activity of Regulatory T Cells.

Jennifer R Dwyer, Jeremy J Racine, Harold D Chapman, Anna Quinlan, Maximiliano Presa, Grace A Stafford, Ingo Schmitz, David V Serreze

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

10 citing papers in PubMed, 12 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Analysis of frequency changes in CD8Diabetology & metabolic syndrome · 2024
    Article
  6. Advancing Animal Models of Human Type 1 Diabetes.Cold Spring Harbor perspectives in medicine · 2024
    Review
  7. Review
  8. Article
  9. Review
  10. 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

8 authors at 2 institutions in 2 countries.

Jennifer R DwyerThe Jackson Laboratory, Bar Harbor, ME; and.ORCID 0000-0002-5893-6026
Jeremy J RacineThe Jackson Laboratory, Bar Harbor, ME; and.ORCID 0000-0001-5514-3074
Harold D ChapmanThe Jackson Laboratory, Bar Harbor, ME; and.
Anna QuinlanThe Jackson Laboratory, Bar Harbor, ME; and.ORCID 0000-0001-8174-5386
Maximiliano PresaThe Jackson Laboratory, Bar Harbor, ME; and.ORCID 0000-0002-0160-6528
Grace A StaffordThe Jackson Laboratory, Bar Harbor, ME; and.ORCID 0000-0001-5707-8165
Ingo SchmitzDepartment of Molecular Immunology, Ruhr-University, Bochum, Germany.ORCID 0000-0002-5360-0419
David V SerrezeThe Jackson Laboratory, Bar Harbor, ME; and dave.serreze@jax.org.ORCID 0000-0001-7614-5925
Jackson Laboratory · USRuhr University Bochum · DE

Funding

Shared Resource ManagementP30CA034196 · NCI · JACKSON LABORATORY · PI William Carl Skarnes · 1985 to 2026
$61.9M
The Jackson Laboratory Center for Precision Genetics: From New Models to Novel TherapeuticsU54OD020351 · OD · JACKSON LABORATORY · PI BURGESS, ROBERT W. · 2015 to 2019
$10.2M
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
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 P30 CA034196NIDDK NIH HHS R01 DK046266NIDDK NIH HHS R01 DK051090NIDDK NIH HHS R01 DK095735NIDDK NIH HHS R29 DK046266NIH HHS U54 OD020351
6 · The paper itself

Abstract

Type 1 diabetes (T1D) in both humans and NOD mice is caused by T cell-mediated autoimmune destruction of pancreatic β cells. Increased frequency or activity of autoreactive T cells and failures of regulatory T cells (Tregs) to control these pathogenic effectors have both been implicated in T1D etiology. Due to the expression of MHC class I molecules on β cells, CD8 T cells represent the ultimate effector population mediating T1D. Developing autoreactive CD8 T cells normally undergo extensive thymic negative selection, but this process is impaired in NOD mice and also likely T1D patients. Previous studies identified an allelic variant of

Indexed as

Diabetes Mellitus, ExperimentalDiabetes Mellitus, Type 1AnimalsCD8-Positive T-LymphocytesHumansMiceMice, Inbred NODMice, TransgenicT-Lymphocytes, Regulatory

Identifiers

PMID35760520
PMCPMC9365269
OpenAlexW4283704967

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.