Evidence map›Paper›PMID 36056148›Full record

ReviewCellular & molecular immunology2022

Redox regulation of the immune response.

Gerwyn Morris, Maria Gevezova, Victoria Sarafian, Michael Maes

Open access · hybridAbstract readReview
In one paragraph

Review in Cellular & molecular immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 304 papers.

0numbers the graph read from it
0cells of the map it votes in
304citing papers in PubMed
55.0field-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

304 citing papers in PubMed, 472 citations in OpenAlex.

  1. Article
  2. Article
  3. IL-17D reprograms CD93Cellular & molecular immunology · 2026
    Article
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  5. Review
  6. Review
  7. Review
  8. Article
  9. Article
  10. Review
  11. Furong Tongmai Capsule Ameliorates Atherosclerosis in ApoEJournal of cellular and molecular medicine · 2026
    Article
  12. Immunomodulatory Nanozymes as Programmable Redox-Immune Set-Point Regulators.Small (Weinheim an der Bergstrasse, Germany) · 2026
    Review
  13. Article
  14. Article
  15. Review
  16. Review
  17. Plasma metabolomics in infancy reveals early signatures of a stringently-defined otitis-prone phenotype.Pediatric allergy and immunology : official publication of the European Society of Pediatric Allergy and Immunology · 2026
    Article
  18. Review
  19. Article
  20. Article

244 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 3 countries.

Gerwyn MorrisDeakin University, IMPACT - the Institute for Mental and Physical Health and Clinical Translation, School of Medicine, Barwon Health, Geelong, VIC, Australia.
Maria GevezovaDepartment of Medical Biology, Medical University-Plovdiv, Plovdiv, Bulgaria.
Victoria SarafianDepartment of Medical Biology, Medical University-Plovdiv, Plovdiv, Bulgaria.
Michael MaesDeakin University, IMPACT - the Institute for Mental and Physical Health and Clinical Translation, School of Medicine, Barwon Health, Geelong, VIC, Australia. dr.michaelmaes@hotmail.com.ORCID http://orcid.org/0000-0002-2012-871X
Barwon Health · AUMedical University Plovdiv · BG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The immune-inflammatory response is associated with increased nitro-oxidative stress. The aim of this mechanistic review is to examine: (a) the role of redox-sensitive transcription factors and enzymes, ROS/RNS production, and the activity of cellular antioxidants in the activation and performance of macrophages, dendritic cells, neutrophils, T-cells, B-cells, and natural killer cells; (b) the involvement of high-density lipoprotein (HDL), apolipoprotein A1 (ApoA1), paraoxonase-1 (PON1), and oxidized phospholipids in regulating the immune response; and (c) the detrimental effects of hypernitrosylation and chronic nitro-oxidative stress on the immune response. The redox changes during immune-inflammatory responses are orchestrated by the actions of nuclear factor-κB, HIF1α, the mechanistic target of rapamycin, the phosphatidylinositol 3-kinase/protein kinase B signaling pathway, mitogen-activated protein kinases, 5' AMP-activated protein kinase, and peroxisome proliferator-activated receptor. The performance and survival of individual immune cells is under redox control and depends on intracellular and extracellular levels of ROS/RNS. They are heavily influenced by cellular antioxidants including the glutathione and thioredoxin systems, nuclear factor erythroid 2-related factor 2, and the HDL/ApoA1/PON1 complex. Chronic nitro-oxidative stress and hypernitrosylation inhibit the activity of those antioxidant systems, the tricarboxylic acid cycle, mitochondrial functions, and the metabolism of immune cells. In conclusion, redox-associated mechanisms modulate metabolic reprogramming of immune cells, macrophage and T helper cell polarization, phagocytosis, production of pro- versus anti-inflammatory cytokines, immune training and tolerance, chemotaxis, pathogen sensing, antiviral and antibacterial effects, Toll-like receptor activity, and endotoxin tolerance.

Indexed as

AntioxidantsNF-kappa BAMP-Activated Protein KinasesAnti-Bacterial AgentsAnti-Inflammatory AgentsAntiviral AgentsApolipoprotein A-IAryldialkylphosphataseCytokinesGlutathioneImmunityLipoproteins, HDLMitogen-Activated Protein KinasesOxidation-ReductionPeroxisome Proliferator-Activated ReceptorsPhosphatidylinositol 3-KinasesAMP-Activated Protein KinasesAnti-Bacterial AgentsAnti-Inflammatory AgentsAntioxidantsAntiviral AgentsApolipoprotein A-IAryldialkylphosphataseCytokinesGlutathioneLipoproteins, HDLMitogen-Activated Protein KinasesNF-kappa BPeroxisome Proliferator-Activated ReceptorsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktReactive Oxygen SpeciesSirolimusThioredoxinsToll-Like ReceptorsAntioxidantsImmune responseInflammationOxidative and nitrosative stressPhysiological stress

Identifiers

PMID36056148
PMCPMC9508259
OpenAlexW4294243416

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.