Evidence map›Paper›PMID 32220307›Full record

ArticleCell metabolism2020

Beta Cell Dedifferentiation Induced by IRE1α Deletion Prevents Type 1 Diabetes.

Hugo Lee, Yong-Syu Lee, Quincy Harenda, Stefan Pietrzak, Hülya Zeynep Oktay, Sierra Schreiber, Yian Liao, Shreyash Sonthalia, Ashley E Ciecko, Yi-Guang Chen and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in Cell metabolism, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 104 papers.

0numbers the graph read from it
0cells of the map it votes in
104citing papers in PubMed
17.4field-weighted citation impact, top 1% 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

104 citing papers in PubMed, 151 citations in OpenAlex.

  1. Deletion of the T1D risk geneBiochemistry and biophysics reports · 2026
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44 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

13 authors at 3 institutions in 1 country.

Hugo LeeDepartment of Biomolecular Chemistry, University of Wisconsin-Madison, School of Medicine and Public Health, Madison, WI 53706, USA.
Yong-Syu LeeDepartment of Biomolecular Chemistry, University of Wisconsin-Madison, School of Medicine and Public Health, Madison, WI 53706, USA.
Quincy HarendaDepartment of Biomolecular Chemistry, University of Wisconsin-Madison, School of Medicine and Public Health, Madison, WI 53706, USA.
Stefan PietrzakDepartment of Cell and Regenerative Biology, Wisconsin Institute for Discovery, Madison, WI 53706, USA.
Hülya Zeynep OktayDepartment of Biomolecular Chemistry, University of Wisconsin-Madison, School of Medicine and Public Health, Madison, WI 53706, USA.
Sierra SchreiberDepartment of Biomolecular Chemistry, University of Wisconsin-Madison, School of Medicine and Public Health, Madison, WI 53706, USA.
Yian LiaoDepartment of Biomolecular Chemistry, University of Wisconsin-Madison, School of Medicine and Public Health, Madison, WI 53706, USA.
Shreyash SonthaliaDepartment of Biomolecular Chemistry, University of Wisconsin-Madison, School of Medicine and Public Health, Madison, WI 53706, USA.
Ashley E CieckoDepartment of Microbiology and Immunology, Medical College of Wisconsin, Milwaukee, WI 53226, USA.
Yi-Guang ChenDepartment of Microbiology and Immunology, Medical College of Wisconsin, Milwaukee, WI 53226, USA; Department of Pediatrics, Medical College of Wisconsin, Milwaukee, WI 53226, USA.
Sunduz KelesDepartment of Biostatistics & Medical Informatics and Department of Statistics, University of Wisconsin-Madison, School of Medicine and Public Health, Madison, WI 53705, USA.
Rupa SridharanDepartment of Cell and Regenerative Biology, Wisconsin Institute for Discovery, Madison, WI 53706, USA.
Feyza EnginDepartment of Biomolecular Chemistry, University of Wisconsin-Madison, School of Medicine and Public Health, Madison, WI 53706, USA; Department of Medicine, Division of Endocrinology, Diabetes & Metabolism, University of Wisconsin-Madison, School of Medicine and Public Health, Madison, WI 53705, USA. Electronic address: fengin@wisc.edu.
University of Wisconsin–Madison · USMedical College of Wisconsin · USWisconsin Institutes for Discovery · US

Funding

UW COMPREHENSIVE CANCER CENTER SUPPORTP30CA014520 · NCI · UNIVERSITY OF WISCONSIN-MADISON · PI Christian Capitini · 1985 to 2026
$142.6M
GRADUATE TRAINING IN MOLECULAR BIOSCIENCEST32GM007215 · NIGMS · UNIVERSITY OF WISCONSIN-MADISON · PI HULL, CHRISTINA M · 1985 to 2018
$22.5M
Institutional Training in the Genomic SciencesT32HG002760 · NHGRI · UNIVERSITY OF WISCONSIN-MADISON · PI Qiongshi Lu · 2003 to 2026
$17.7M
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
Statistical Methods for the Analysis of ChlP-chip DataR01HG003747 · NHGRI · UNIVERSITY OF WISCONSIN-MADISON · PI KELES, SUNDUZ · 2007 to 2024
$4.8M
R01 Renewal: Collaboration of chromatin remodeling and signaling pathways in pluripotencyR01GM113033 · NIGMS · UNIVERSITY OF WISCONSIN-MADISON · PI SRIDHARAN, RUPA · 2015 to 2023
$2.9M
Shaping diabetogenic T cells by IL-27 in type 1 diabetesR01DK121747 · NIDDK · MEDICAL COLLEGE OF WISCONSIN · PI CHEN, YI-GUANG · 2019 to 2022
$1.5M
Genetic analysis of islet-infiltrating IL-21-expressing CD4 T cells in type 1 diabetesR21AI144360 · NIAID · MEDICAL COLLEGE OF WISCONSIN · PI CHEN, YI-GUANG · 2020 to 2021
$418k
Beta cell endoplasmic reticulum stress and its crosstalk with immune system in tyK01DK102488 · NIDDK · UNIVERSITY OF WISCONSIN-MADISON · PI ENGIN, FEYZA · 2014 to 2016
$356k
The role of IL-27 signaling in the accumulation and sustained effector function of autoreactive CD8 T cells in type 1 diabetesF31DK118786 · NIDDK · MEDICAL COLLEGE OF WISCONSIN · PI CIECKO, ASHLEY · 2019 to 2020
$82k
NCI NIH HHS P30 CA014520NHGRI NIH HHS R01 HG003747NHGRI NIH HHS T32 HG002760NIAID NIH HHS R21 AI144360NIDDK NIH HHS F31 DK118786NIDDK NIH HHS K01 DK102488NIDDK NIH HHS R01 DK107541NIDDK NIH HHS R01 DK121747NIGMS NIH HHS R01 GM113033NIGMS NIH HHS T32 GM007215
6 · The paper itself

Abstract

Immune-mediated destruction of insulin-producing β cells causes type 1 diabetes (T1D). However, how β cells participate in their own destruction during the disease process is poorly understood. Here, we report that modulating the unfolded protein response (UPR) in β cells of non-obese diabetic (NOD) mice by deleting the UPR sensor IRE1α prior to insulitis induced a transient dedifferentiation of β cells, resulting in substantially reduced islet immune cell infiltration and β cell apoptosis. Single-cell and whole-islet transcriptomics analyses of immature β cells revealed remarkably diminished expression of β cell autoantigens and MHC class I components, and upregulation of immune inhibitory markers. IRE1α-deficient mice exhibited significantly fewer cytotoxic CD8

Indexed as

Cell DedifferentiationInsulin-Secreting CellsUnfolded Protein ResponseAnimalsCD8-Positive T-LymphocytesDiabetes Mellitus, Type 1EndoribonucleasesGene DeletionHyperglycemiaMiceMice, Inbred NODMice, KnockoutProtein Serine-Threonine KinasesEndoribonucleasesErn1 protein, mouseProtein Serine-Threonine Kinasesbeta celldedifferentiationER stressIRE1isletNODRNA-seqsingle celltype 1 diabetesUPR

Identifiers

PMID32220307
PMCPMC7346095
OpenAlexW3013062548

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.