Evidence map›Paper›PMID 30809228›Full record

ReviewFrontiers in immunology2019

TET Enzymes and 5hmC in Adaptive and Innate Immune Systems.

Chan-Wang J Lio, Anjana Rao

Registry-linked trialAbstract 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. It is linked to trial NCT04766814 (Epigenetic Analysis of Regulation of the Inflammasome-activating NLRP3 Gene in Monocytes From Atrial Fibrillation Patients and Controls), which is not on this map. Cited by 79 papers.

0numbers the graph read from it
0cells of the map it votes in
79citing papers in PubMed
–field-weighted citation impact
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.

NCT04766814 completednot on this mapstarted 2021, after this paper: background citation

Epigenetic Analysis of Regulation of the Inflammasome-activating NLRP3 Gene in Monocytes From Atrial Fibrillation Patients and Controls

TypeobservationalSponsorTulane UniversityRan2021 to 2024Enrolled29ConditionsAtrial Fibrillation, Arrhythmia
3 · Its place in the literature

Who cites it

79 citing papers in PubMed.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Review
  6. TET1 deficiency amplifies macrophage inflammatory signaling associated with Crohn's disease.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Article
  7. Review
  8. Article
  9. Review
  10. Review
  11. Review
  12. Review
  13. SilencingEnvironmental epigenetics · 2025
    Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. DNA methylation modification in Idiopathic pulmonary fibrosis.Frontiers in cell and developmental biology · 2024
    Review
  20. Review

19 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

2 authors.

Chan-Wang J LioDivision of Signaling and Gene Expression, La Jolla Institute, La Jolla, CA, United States.
Anjana RaoDivision of Signaling and Gene Expression, La Jolla Institute, La Jolla, CA, United States.

Funding

The TET-DNMT-ASXL1-OGT axis: relevance to clonal hematopoiesis, heterochromatin integrity and cancerR35CA210043 · NCI · LA JOLLA INSTITUTE FOR IMMUNOLOGY · PI Anjana Rao · 2016 to 2026
$10.6M
NFAT, bZIP proteins, and transcriptional programs in lymphocytesR01AI109842 · NIAID · LA JOLLA INSTITUTE FOR IMMUNOLOGY · PI Patrick Hogan, Anjana Rao · 2014 to 2026
$8.6M
Investigating the role of TET deficiency in promoting T cell expansion and inflammationR01AI128589 · NIAID · LA JOLLA INSTITUTE FOR IMMUNOLOGY · PI RAO, ANJANA · 2017 to 2025
$5.3M
NFAT, bZIP proteins, and transcriptional programs in lymphocytesR56AI109842 · NIAID · LA JOLLA INSTITUTE FOR IMMUNOLOGY · PI HOGAN, PATRICK, RAO, ANJANA · 2019 to 2019
$414k
NCI NIH HHS R35 CA210043NIAID NIH HHS R01 AI109842NIAID NIH HHS R01 AI128589NIAID NIH HHS R56 AI109842
6 · The paper itself

Abstract

DNA methylation is an abundant and stable epigenetic modification that allows inheritance of information from parental to daughter cells. At active genomic regions, DNA methylation can be reversed by TET (Ten-eleven translocation) enzymes, which are responsible for fine-tuning methylation patterns. TET enzymes oxidize the methyl group of 5-methylcytosine (5mC) to yield 5-hydroxymethylcytosine (5hmC) and other oxidized methylcytosines, facilitating both passive and active demethylation. Increasing evidence has demonstrated the essential functions of TET enzymes in regulating gene expression, promoting cell differentiation, and suppressing tumor formation. In this review, we will focus on recent discoveries of the functions of TET enzymes in the development and function of lymphoid and myeloid cells. How TET activity can be modulated by metabolites, including vitamin C and 2-hydroxyglutarate, and its potential application in shaping the course of immune response will be discussed.

Indexed as

Adaptive ImmunityImmunity, Innate5-MethylcytosineAnimalsBiomarkersCell DifferentiationDNA-Binding ProteinsDNA MethylationEnzymesEpigenesis, GeneticGene Expression RegulationHumansLymphocyte SubsetsProto-Oncogene Proteins5-hydroxymethylcytosine5-MethylcytosineBiomarkersDNA-Binding ProteinsEnzymesProto-Oncogene Proteins5hmC5 hydroxymethylcytosineDNA modificationepigenetics (methylation/demethylation)gene regulation and expressionten eleven translocation (TET)

Identifiers

PMID30809228
PMCPMC6379312

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Registered trials

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.