Caspian journal of internal medicine · 2025
Reshape memory T cell landscape in CML patients' blood by tyrosine kinase inhibitors.
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Kareem Haneen Ali, Ghadi Haydar Hassan
Аннотация
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.
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.