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December 8, 2025BloodOpen Access

TET2 mutations drive cell-autonomous type I interferon production and selective advantage through TRIM4 silencing

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Authors

MJManon JaudLTLewis E. TomalinCFChih-Wei Fan

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Overview

Observational analysis revealed that TET2 mutations enhance type I interferon production in HSPCs, suggesting a potential therapeutic target via TRIM4 silencing.

Key Points

  • TET2 mutations lead to increased production of type I interferon, promoting a pro-inflammatory environment.
  • The study identified a critical role for TRIM4 silencing in mediating the effects of TET2 deficiency.
  • Analysis included integrated transcriptome and proteomics to uncover pathways in clonal hematopoiesis.
  • Blocking interferon signaling may mitigate the clonal advantage provided by TET2 mutations.

Cite This Study

Jaud et al. (2025) studied this question.

synapsesocial.com/papers/69362f764fa91c937236e36dhttps://doi.org/10.1182/blood-2025-976
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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Perturbation of iNKT differentiation during clonal hematopoiesis from rewiring of inflammation and lipid presentation2025
  2. 2Chromodomain helicase DNA binding protein CHD2 interacts with TET2 and regulates lineage defining transcription in hematopoietic stem and progenitor cells2025
  3. 3Single-cell multiomic profiling of gene mutation, chromatin accessibility, and gene expression in TET2-mutant clonal hematopoiesis2025
  4. 4Accelerated adverse cardiac remodeling in a model of TET2 mutation-driven clonal hematopoiesis is ameliorated by IFNa treatment by modulating the monocyte response2025
  5. 5Loss of TET function in T regulatory cells yields ex-Treg cells biased toward T follicular helper cells, causing autoimmune diseases through autoantibody production2025 · 1 citations