ArticleCaspian journal of internal medicine2025
Reshape memory T cell landscape in CML patients' blood by tyrosine kinase inhibitors.
Article in Caspian journal of internal medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: CML, a blood cancer characterized by excessive myeloid cell proliferation, stems from the BCR-ABL1 gene fusion. This research aimed to uncover why leukemic stem cells resist treatment and explore innovative immune-based therapies to improve patient outcomes. Methods: This study investigated the immunologic phenotypes (CD8, CD27, CD197, and CD45RA) of T cell subsets (TN, TCM, TEM, and TEF) in the peripheral blood of chronic myeloid leukemia patients in the chronic phase who achieved a complete molecular response to tyrosine kinase inhibitors. The treatment-free remission (TFR) patients were compared to age- and gender-matched healthy volunteers using multicolor flow cytometry for analysis. Results: Flow cytometry analysis unveiled notable shifts in CD8+ T cell subsets. CML-CP patients showed a marked decrease in central memory T cells (TCM), dropping to 7.2% of the CD8+ population. Conversely, these patients exhibited substantial increases in effector memory T (TEM) and effector T (TEF) cells, rising to 37.6% and 24.4% respectively. The most statistically significant change occurred in the CD8+ TEF subset. CML-CP patients displayed a 24.4% presence of these cells, compared to only 15.7% in control groups. These findings suggest a distinct immunological profile in CML-CP, potentially impacting disease progression and treatment strategies. Conclusion: Tyrosine kinase inhibitors restore the distribution of memory T cells in patients with chronic myeloid leukemia (CML), but T cell exhaustion remains an issue. This situation highlights the need for alternative activation strategies to enhance immunity.
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