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December 8, 2025BloodOpen Access

Impact of innate immune memory on MDS progression by TET2-driven inflammation

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Authors

XDXenia DavisSZSandra S. Zinkel

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Overview

Findings indicate TET2 deficiency impairs infection response in MDS, linking innate immune memory to inflammation outcomes.

Key Points

  • This research aims to investigate how TET2 deficiency and innate immune memory influence inflammation and MDS progression.
  • Utilized vavTet2fl/fl and vavTet2fl/flRipk1D138N/+ mouse models.
  • Applied Pseudomonas aeruginosa sepsis model.
  • Administered MPLA to assess immune response improvements.
  • Conducted spectral flow cytometry to evaluate immune cell differentiation.
  • TET2-deficient mice displayed impaired responses to infection compared to wild-type controls.
  • MPLA pretreatment provided incomplete protection against infection in TET2-deficient mice.
  • Observed reductions in reactive oxygen species (ROS) production and phagocytosis in TET2-deficient groups.
  • Significant myeloid-biased differentiation in bone marrow of TET2-deficient mice was noted.

Cite This Study

Davis et al. (2025) studied this question.

synapsesocial.com/papers/693624dd4fa91c937236d243https://doi.org/10.1182/blood-2025-1400
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Also Consider

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

  1. 1TET2 loss impairs MPLA-induced innate immune memory during infection and disrupts hematopoiesis via RIPK1 in mice2025
  2. 2Mavs mediates inflammatory memory in hematopoietic stem cells and promotes ineffective hematopoiesis2025
  3. 3Accelerated adverse cardiac remodeling in a model of TET2 mutation-driven clonal hematopoiesis is ameliorated by IFNa treatment by modulating the monocyte response2025
  4. 4The bromodomain and extra-terminal domain protein BRD4 promotes both self renewal and inflammation in TET2 mutated clonal hematopoiesis2025
  5. 5Perturbation of iNKT differentiation during clonal hematopoiesis from rewiring of inflammation and lipid presentation2025