ArticleNature communications2022
CD4 expression in effector T cells depends on DNA demethylation over a developmentally established stimulus-responsive element.
Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 13 citations in OpenAlex.
- T cell exhaustion in parasitic infections.Frontiers in immunology · 2026Review
- The TET-TDG axis in T cells and biological processes.International immunology · 2025Review
- GlyT1 inhibition by ALX-5407 attenuates allograft rejection through suppression of Th1 cell differentiation.Frontiers in immunology · 2025Article
- T-follicular helper cells are epigenetically poised to transdifferentiate into T-regulatory type 1 cells.eLife · 2024Article
- Article
- DNA demethylation fine-tunes IL-2 production during thymic regulatory T cell differentiation.EMBO reports · 2023Article
- Canine diabetes mellitus demonstrates multiple markers of chronic inflammation including Th40 cell increases and elevated systemic-immune inflammation index, consistent with autoimmune dysregulation.Frontiers in immunology · 2023Article
- TET Proteins in the Spotlight: Emerging Concepts of Epigenetic Regulation in T Cell Biology.ImmunoHorizons · 2023Article
- TET proteins regulate T cell and iNKT cell lineage specification in a TET2 catalytic dependent manner.Frontiers in immunology · 2022Article
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
Abstract
The epigenetic patterns that are established during early thymic development might determine mature T cell physiology and function, but the molecular basis and topography of the genetic elements involved are not fully known. Here we show, using the Cd4 locus as a paradigm for early developmental programming, that DNA demethylation during thymic development licenses a novel stimulus-responsive element that is critical for the maintenance of Cd4 gene expression in effector T cells. We document the importance of maintaining high CD4 expression during parasitic infection and show that by driving transcription, this stimulus-responsive element allows for the maintenance of histone H3K4me3 levels during T cell replication, which is critical for preventing de novo DNA methylation at the Cd4 promoter. A failure to undergo epigenetic programming during development leads to gene silencing during effector T cell replication. Our study thus provides evidence of early developmental events shaping the functional fitness of mature effector T cells.
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Registered trials
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