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December 8, 2025BloodOpen Access

Pediatric Acute Myeloid Leukemia associated S100A9 promotes T cell dysfunction

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Authors

ZYZhiyuan YouMLMatthew LearBYBen Youngblood

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Overview

Analysis reveals increased T cell dysfunction and altered DNA methylation in myeloid malignancies, indicating S100A9's role in immune suppression.

Key Points

  • T cell dysfunction was significantly associated with changes in DNA methylation in pediatric AML.
  • Cytotoxicity and epigenetic regulation were disrupted in T cells from AML patients compared to ALL.
  • Phenotypic analysis indicated a terminal effector phenotype in AML-derived T cells, impairing their function.
  • These findings highlight the complex interplay between T cells and the myeloid tumor microenvironment, warranting further exploration.

Cite This Study

You et al. (2025) studied this question.

synapsesocial.com/papers/69362f6e4fa91c937236e0a2https://doi.org/10.1182/blood-2025-1725
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Also Consider

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

  1. 1S100A8/A9 drives T cell exhaustion and compromises the therapeutic efficacy of bispecific antibodies in multiple myeloma.2025
  2. 2Comprehensive profiling of the bone marrow microenvironment reveals an exhausted immune signature associated with tumor burden in Acute Myeloid Leukemia2025
  3. 3The Acute Myeloid Leukemia microenvironment is defined by ineffective immune surveillance despite the presence of activated, clonally-expanded CD8 T cells with preserved effector function2025
  4. 4Monoclonal antibodies against pathogenic S100A8/9 alarmins can restore hematopoiesis and result in immunomodulation in myelodysplasia and leukemia models2025
  5. 5Dynamics of leukemic blast and immune cell populations in Acute Myeloid Leukemia2025