Evidence map›Paper›PMID 30230178›Full record

ReviewDiabetes, obesity & metabolism2018

Islet stress, degradation and autoimmunity.

Sofia Thomaidou, Arnaud Zaldumbide, Bart O Roep

Open access · hybridAbstract readReview
In one paragraph

Review in Diabetes, obesity & metabolism, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

31 citing papers in PubMed, 47 citations in OpenAlex.

  1. Article
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  6. Article
  7. Applications of Genome-Editing Technologies for Type 1 Diabetes.International journal of molecular sciences · 2023
    Review
  8. Article
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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

3 authors at 1 institution in 2 countries.

Sofia ThomaidouDepartment of Cell and Chemical Biology, Leiden University Medical Center, Leiden, The Netherlands.
Arnaud ZaldumbideDepartment of Cell and Chemical Biology, Leiden University Medical Center, Leiden, The Netherlands.ORCID 0000-0001-6680-4456
Bart O RoepDepartment of Immunohematology and Blood bank Leiden University Medical Center, Leiden University Medical Center, Leiden, The Netherlands.ORCID 0000-0002-3110-7391
Leiden University Medical Center · NL

Funding

Diabetes FondsDON foundation stichting DON (Diabetes Onderzoek Nederland)Juvenile Diabetes Research Foundation
6 · The paper itself

Abstract

β-cell destruction in type 1 diabetes (T1D) results from the effect of inflammation and autoimmunity. In response to inflammatory signals, islet cells engage adaptive mechanisms to restore and maintain cellular homeostasis. Among these mechanisms, the unfolded protein response (UPR) leads to a reduction of the general protein translation rate, increased production of endoplasmic reticulum chaperones and the initiation of degradation by activation of the ER associated degradation pathway (ERAD) in which newly synthetized proteins are ubiquitinylated and processed through the proteasome. This adaptive phase is also believed to play a critical role in the development of autoimmunity by the generation of neoantigens. While we have previously investigated the effect of stress on transcription, translation and post-translational events as possible source for neoantigens, the participation of the degradation machinery, yet crucial in the generation of antigenic peptides, remains to be investigated in the context of T1D pathology. In this review, we will describe the relation between the unfolded protein response and the Ubiquitin Proteasome System (UPS) and address the role of the cellular degradation machinery in the generation of antigens. Learning from tumour immunology, we propose how these processes may unmask β-cells by triggering the generation of aberrant peptides recognized by the immune cells.

Indexed as

AutoimmunityDiabetes Mellitus, Type 1Endoplasmic Reticulum StressHumansInsulinIslets of LangerhansProteasome Endopeptidase ComplexInsulinProteasome Endopeptidase ComplexautoimmunityER stressneoantigenproteasomeβ-cell

Identifiers

PMID30230178
PMCPMC6174957
OpenAlexW2891590598

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.