ArticleJCI insight2022
TET2 regulates immune tolerance in chronically activated mast cells.
Article in JCI insight, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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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.
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Who cites it
7 citing papers in PubMed, 9 citations in OpenAlex.
- Case report: A case of mast cell leukemia treated with avapritinib: from diagnostic challenge to transplantation.Frontiers in oncology · 2026Article
- Molecular characterization of pediatric mastocytosis revealed different somatic mutations with uncertain prognostic value.Frontiers in cell and developmental biology · 2026Article
- Crosstalk between metabolism and epigenetics during macrophage polarization.Epigenetics & chromatin · 2025Review
- Functional heterogeneity of mast cells in cutaneous inflammation: implications for precision medicine.Frontiers in immunology · 2025Review
- Potential Role of Moesin in Regulating Mast Cell Secretion.International journal of molecular sciences · 2023Review
- The Role of Inflammation in the Initiation and Progression of Myeloid Neoplasms.Blood cancer discovery · 2023Article
- Innate immunity in pancreatic cancer: Lineage tracing and function.Frontiers in immunology · 2022Review
Corrections and comments
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Authors and funding
18 authors at 3 institutions in 3 countries.
Funding
Abstract
Mutation of the TET2 DNA-hydroxymethylase has been associated with a number of immune pathologies. The disparity in phenotype and clinical presentation among these pathologies leads to questions regarding the role of TET2 mutation in promoting disease evolution in different immune cell types. Here we show that, in primary mast cells, Tet2 expression is induced in response to chronic and acute activation signals. In TET2-deficient mast cells, chronic activation via the oncogenic KITD816V allele associated with mastocytosis, selects for a specific epigenetic signature characterized by hypermethylated DNA regions (HMR) at immune response genes. H3K27ac and transcription factor binding is consistent with priming or more open chromatin at both HMR and non-HMR in proximity to immune genes in these cells, and this signature coincides with increased pathological inflammation signals. HMR are also associated with a subset of immune genes that are direct targets of TET2 and repressed in TET2-deficient cells. Repression of these genes results in immune tolerance to acute stimulation that can be rescued with vitamin C treatment or reiterated with a Tet inhibitor. Overall, our data support a model where TET2 plays a direct role in preventing immune tolerance in chronically activated mast cells, supporting TET2 as a viable target to reprogram the innate immune response for innovative therapies.
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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.