Natural killer T lymphocyte like cells function and cytokine production interferon γ and interleukin 10 in chronic myelogenous leukemia: Implications for immune surveillance

Abstract: BACKGROUND: Chronic myeloid leukemia (CML) is driven by the BCR-ABL1 oncogene (t(9;22)) and typically presents in a chronic phase (<10% of blasts). Immune dysfunction in CML includes impaired natural killer-like T (NKT) cells, while NKT-like cells increase with age. Interferon-gamma (IFN-γ), crucial for immunity, activates JAK-STAT signaling, with dysregulation linked to disease. OBJECTIVE: The study aimed to analyze the immunological parameters (NKT-like cells, INF-γ, and interleukin-10 [IL-10]) in CML patients. MATERIALS AND METHODS: The study comprised 60 individuals: 20 with newly diagnosed CML and 40 who were undergoing treatment with TKIs. The present research, which took place from February to September 2025, utilized flow cytometry to measure NKT-like cells. In addition, an enzyme-linked immunosorbent assay was employed to measure the levels of key cytokines, including IFN-γ and IL-10, in patient samples. RESULTS: Newly diagnosed CML patients showed depletion of NKT-like cells and IFN-γ but high levels of IL-10. Controls had higher NKT-like cells (57.5%) than untreated CML (26.1%), with partial recovery posttreatment (51.7%). IFN-γ was elevated in controls (22.6 pg/ml), while IL-10 dominated in untreated CML (49.6 pg/ml). Significant CML correlations revealed NKT-like cells negatively associated with blast ( r = −0.651) and BCR-ABL levels ( r = −0.547) while showing a positive correlation with IFN-γ ( r = 0.460). Conversely, IL-10 positively correlated with (blasts: r = 0.380 and BCR-ABL: r = 0.617) but negatively with NKT cells ( r = −0.276). CONCLUSION: The current study reveals profound immune dysregulation in CML, marked by decreased NKT-like cells and IFN-γ alongside elevated IL-10, particularly in untreated patients. These findings support the known BCR-ABL1-mediated impairment of NKT function, highlighting key mechanisms of immune escape in CML pathogenesis.