Evidence map›Paper›PMID 29556237›Full record

ReviewFrontiers in immunology2018

Regulation of Cytokine Production by the Unfolded Protein Response; Implications for Infection and Autoimmunity.

Judith A Smith

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 111 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
111citing papers in PubMed, 1 pooled it
8.9field-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

111 citing papers in PubMed, 1 synthesis or guideline pooled it, 164 citations in OpenAlex.

  1. Guideline
  2. Review
  3. Dual role of homocysteine in enhancing metabolic activity and suppressing inflammatory cytokines in murine immune cells.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2026
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  20. Human coronaviruses: activation and antagonism of innate immune responses.Microbiology and molecular biology reviews : MMBR · 2025
    Review

51 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

1 author at 1 institution in 1 country.

Judith A SmithDepartment of Pediatrics, University of Wisconsin-Madison School of Medicine and Public Health, Madison, WI, United States.
University of Wisconsin–Madison · US

Funding

Brucella epitope recognition by CD8+ T cellsR01AI073558 · NIAID · UNIVERSITY OF WISCONSIN-MADISON · PI HARMS, JEROME SCOTT, SMITH, JUDITH ANNE · 2008 to 2016
$3.3M
Brucella survival strategy requires endoplasmic reticulum restructuring and interferes with innate immunityR01AI116453 · NIAID · FOUNDATION FOR RESEARCH DEVELOPMENT · PI BARBER, GLEN N, OLIVEIRA, SERGIO C · 2016 to 2025
$1.4M
Regulation of human immune function by 17q21 asthma risk polymorphismR21AI121808 · NIAID · UNIVERSITY OF WISCONSIN-MADISON · PI SMITH, JUDITH ANNE · 2016 to 2017
$421k
NIAID NIH HHS R01 AI073558NIAID NIH HHS R01 AI116453NIAID NIH HHS R21 AI121808
6 · The paper itself

Abstract

Protein folding in the endoplasmic reticulum (ER) is an essential cell function. To safeguard this process in the face of environmental threats and internal stressors, cells mount an evolutionarily conserved response known as the unfolded protein response (UPR). Invading pathogens induce cellular stress that impacts protein folding, thus the UPR is well situated to sense danger and contribute to immune responses. Cytokines (inflammatory cytokines and interferons) critically mediate host defense against pathogens, but when aberrantly produced, may also drive pathologic inflammation. The UPR influences cytokine production on multiple levels, from stimulation of pattern recognition receptors, to modulation of inflammatory signaling pathways, and the regulation of cytokine transcription factors. This review will focus on the mechanisms underlying cytokine regulation by the UPR, and the repercussions of this relationship for infection and autoimmune/autoinflammatory diseases. Interrogation of viral and bacterial infections has revealed increasing numbers of examples where pathogens induce or modulate the UPR and implicated UPR-modulated cytokines in host response. The flip side of this coin, the UPR/ER stress responses have been increasingly recognized in a variety of autoimmune and inflammatory diseases. Examples include monogenic disorders of ER function, diseases linked to misfolding protein (HLA-B27 and spondyloarthritis), diseases directly implicating UPR and autophagy genes (inflammatory bowel disease), and autoimmune diseases targeting highly secretory cells (e.g., diabetes). Given the burgeoning interest in pharmacologically targeting the UPR, greater discernment is needed regarding how the UPR regulates cytokine production during specific infections and autoimmune processes, and the relative place of this interaction in pathogenesis.

Indexed as

AnimalsAutoimmunityCytokinesDiabetes ComplicationsEndoplasmic ReticulumHumansInfectionsInflammationInflammatory Bowel DiseasesReceptors, Pattern RecognitionSpondylitis, AnkylosingUnfolded Protein ResponseCytokinesReceptors, Pattern Recognitionautoimmunityautoinflammatory diseasebacteriacytokine regulationendoplasmic reticulum stressinfectionunfolded protein responsevirus

Identifiers

PMID29556237
PMCPMC5844972
OpenAlexW2789523895

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.