Evidence map›Paper›PMID 32868408›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2020

CD70 Inversely Regulates Regulatory T Cells and Invariant NKT Cells and Modulates Type 1 Diabetes in NOD Mice.

Cheng Ye, Benjamin E Low, Michael V Wiles, Todd M Brusko, David V Serreze, John P Driver

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.5field-weighted citation impact, top 38% 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

5 citing papers in PubMed, 10 citations in OpenAlex.

  1. Article
  2. Multi-omics investigation of prospective therapeutic targets for type 1 diabetes.Therapeutic advances in endocrinology and metabolism · 2025
    Article
  3. Review
  4. Article
  5. Review
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 2 institutions in 1 country.

Cheng YeDepartment of Animal Sciences, University of Florida, Gainesville, FL 32611.
Benjamin E LowThe Jackson Laboratory, Bar Harbor, ME 04609; and.
Michael V WilesThe Jackson Laboratory, Bar Harbor, ME 04609; and.ORCID 0000-0002-3620-8386
Todd M BruskoDepartment of Pathology, Immunology and Laboratory Medicine, University of Florida Diabetes Institute, Gainesville, FL 32610.ORCID 0000-0003-2878-9296
David V SerrezeThe Jackson Laboratory, Bar Harbor, ME 04609; and.ORCID 0000-0001-7614-5925
John P DriverDepartment of Animal Sciences, University of Florida, Gainesville, FL 32611; jdriver@ufl.edu.ORCID 0000-0002-6714-3335
Jackson Laboratory · USUniversity of Florida · US

Funding

Project 3P01AI042288 · NIAID · UNIVERSITY OF FLORIDA · PI Todd Michael Brusko · 1997 to 2026
$32.9M
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
The CD226 costimulatory axis in type 1 diabetesR01DK106191 · NIDDK · UNIVERSITY OF FLORIDA · PI Todd Michael Brusko · 2016 to 2026
$4.4M
Genetic control of autoimmune diabetes inducing cytotoxic T cellsR21AI130656 · NIAID · UNIVERSITY OF FLORIDA · PI CHEN, YI-GUANG, DRIVER, JOHN · 2018 to 2019
$420k
DIABETOGENIC ROLE OF H-2G7 CLASS I ALLELES IN NOD MICER29DK046266 · NIDDK · JACKSON LABORATORY · PI SERREZE, DAVID V. · 1993 to 1998
–
NIAID NIH HHS HHSN272201300006CNIAID NIH HHS P01 AI042288NIAID NIH HHS R21 AI130656NIDDK NIH HHS R01 DK046266NIDDK NIH HHS R01 DK095735NIDDK NIH HHS R01 DK106191NIDDK NIH HHS R29 DK046266NIH HHS U54 OD020351
6 · The paper itself

Abstract

The CD27-CD70 costimulatory pathway is essential for the full activation of T cells, but some studies show that blocking this pathway exacerbates certain autoimmune disorders. In this study, we report on the impact of CD27-CD70 signaling on disease progression in the NOD mouse model of type 1 diabetes (T1D). Specifically, our data demonstrate that CD70 ablation alters thymocyte selection and increases circulating T cell levels. CD27 signaling was particularly important for the thymic development and peripheral homeostasis of Foxp3

Indexed as

AnimalsCD27 LigandCell DifferentiationDiabetes Mellitus, Type 1Disease Models, AnimalDNA-Binding ProteinsForkhead Transcription FactorsHumansImmunomodulationLymphocyte ActivationMiceMice, Inbred NODMice, KnockoutNatural Killer T-CellsSignal TransductionT-Lymphocytes, RegulatoryCD27 LigandDNA-Binding ProteinsForkhead Transcription FactorsFoxp3 protein, mouseTranscription FactorsTumor Necrosis Factor Receptor Superfamily, Member 7Zfpn1a2 protein, mouse

Identifiers

PMID32868408
PMCPMC7787366
OpenAlexW3081552534

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.