Hematology ·
Abnormal stromal cells impair NK-cell function in MDS and secondary AML
A study published in *Leukemia* examined how mesenchymal stromal cells from people with myelodysplastic neoplasms (MDS) and secondary acute myeloid leukemia (sAML) affect natural killer (NK) cells. Integrated gene-expression and chromatin-accessibility profiling linked pathological stromal cells to mitochondrial damage, apoptosis and reduced NK-cell cytotoxic activity.
- Disease-associated MSCs impaired NK-cell cytotoxic activity.
- Profiling showed altered chromatin accessibility and gene expression.
- Mitochondrial fragmentation and apoptosis were reported.
- Mitochondrial resilience is a proposed research direction.
The study investigated whether mesenchymal stromal cells (MSCs) from patients with MDS and sAML alter NK-cell anti-leukemic function. Researchers used integrated ATAC-seq and RNA-seq profiling to characterize changes in NK cells exposed to disease-associated MSCs. The supplied text does not report the sample size or other quantitative results.
Compared with the supportive effects attributed to healthy MSCs, pathological MSCs were associated with reduced promoter accessibility and lower expression of genes involved in NK-cell stress response and survival. They also induced mitochondrial fragmentation and apoptosis, with a resulting reduction in NK-cell cytotoxic activity.
The findings suggest that disease-associated bone marrow stromal cells may contribute to impaired immune surveillance in MDS and sAML. The authors propose that strategies to support mitochondrial resilience in NK cells could be investigated, but the reported findings do not establish a treatment or clinical benefit. The available source provides no sample-size details or quantitative effect estimates, and the proposed therapeutic approach remains exploratory.
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Leukemia: Mesenchymal stromal cells drive immune escape in MDS and sAML through metabolic rewiring of NK cells ↗This is an automated AI-condensed summary that has not yet been reviewed by an editor. Always consult the full item at the original source.