Evidence map›Paper›PMID 32117210›Full record

ReviewFrontiers in immunology2019

The Emerging Roles of Endoplasmic Reticulum Stress in Balancing Immunity and Tolerance in Health and Diseases: Mechanisms and Opportunities.

Anqi Li, No-Joon Song, Brian P Riesenberg, Zihai Li

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed
7.4field-weighted citation impact, top 2% 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

67 citing papers in PubMed, 120 citations in OpenAlex.

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  10. CNPY2 drives DSS-induced colitis via the macrophage-ROS axis.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2025
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7 more citing papers are in PubMed but not listed here.

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 1 country.

Anqi LiCollege of Medicine, The Ohio State University, Columbus, OH, United States.
No-Joon SongThe James Comprehensive Cancer Center, Pelotonia Institute for Immuno-Oncology, The Ohio State University, Columbus, OH, United States.
Brian P RiesenbergThe James Comprehensive Cancer Center, Pelotonia Institute for Immuno-Oncology, The Ohio State University, Columbus, OH, United States.
Zihai LiCollege of Medicine, The Ohio State University, Columbus, OH, United States.
The Ohio State University · USThe Ohio State University Comprehensive Cancer Center – Arthur G. James Cancer Hospital and Richard J. Solove Research Institute · US

Funding

Project 3: Structural Basis for grp94 Drug Development and Chaperone FunctionP01CA186866 · NCI · OHIO STATE UNIVERSITY · PI LI, ZIHAI · 2015 to 2019
$6.7M
Molecular chaperones and immune toleranceR01AI077283 · NIAID · UNIVERSITY OF CONNECTICUT SCH OF MED/DNT · PI LI, ZIHAI · 2009 to 2021
$3.7M
Integration of inflammation and cancer by molecular chaperoneR01CA213290 · NCI · OHIO STATE UNIVERSITY · PI LI, ZIHAI · 2017 to 2021
$860k
NCI NIH HHS P01 CA186866NCI NIH HHS R01 CA213290NIAID NIH HHS R01 AI077283
6 · The paper itself

Abstract

The endoplasmic reticulum (ER) is an organelle equipped with mechanisms for proper protein folding, trafficking, and degradation to maintain protein homeostasis in the secretory pathway. As a defense mechanism, perturbation of ER proteostasis by ER stress agents activates a cascade of signaling pathways from the ER to the nucleus known as unfolded protein response (UPR). The primary goal of UPR is to induce transcriptional and translational programs to restore ER homeostasis for cell survival. As such, defects in UPR signaling have been implicated as a key contributor to multiple diseases including metabolic diseases, degenerative diseases, inflammatory disorders, and cancer. Growing evidence support the critical role of ER stress in regulating the fate as well as the magnitude of the immune response. Moreover, the availability of multiple UPR pharmacological inhibitors raises the hope that targeting UPR can be a new strategy for immune modulation and immunotherapy of diseases. This paper reviews the principal mechanisms by which ER stress affects immune cell biology and function, with a focus of discussion on UPR-associated immunopathology and the development of potential ER stress-targeted therapeutics.

Indexed as

AnimalsEndoplasmic Reticulum StressHomeostasisHumansImmune ToleranceImmunityUnfolded Protein Responsediseasesendoplasmic reticulum stressimmunityinhibitorstherapeutics

Identifiers

PMID32117210
PMCPMC7026265
OpenAlexW3005615488

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.