Evaluation of programmed death-ligand 2 gene expression level and myeloid-derived suppressor cells% in newly diagnosed acute myeloid leukemia patients

Abstract

Background Acute myeloid leukemia (AML) is a hematological malignancy characterized by clonal expansion of myeloid blasts and impaired hematopoiesis. Immune evasion mechanisms, including increased myeloid-derived suppressor cells (MDSCs) and upregulation of immune checkpoint ligands such as programmed death-ligand 2 (PDL2), may contribute to treatment resistance and poor prognosis in AML. Aim To evaluate the expression levels of PDL2 and the percentage of MDSCs in newly diagnosed AML patients and to correlate these markers with treatment response and genetic risk profiles. Patients and methods A case–control study was conducted involving 50 newly diagnosed AML patients and 50 healthy controls at the Hematology Departments of Kafr El-Sheikh University Hospitals. Flow cytometry was used to measure MDSC percentages and PDL2 expression. Patients were followed up on treatment response on day 28. Correlations with response categories and molecular/cytogenetic risk factors were analyzed. Results MDSC% and PDL2 expression were significantly elevated in nonresponders and deceased patients compared to responders. A strong positive correlation was found between MDSC% and PDL2 among nonresponders. receiver operating characteristic analysis revealed excellent predictive performance of both PDL2 (area under the curve=0.950) and MDSC% (area under the curve=1.0) for distinguishing responders from nonresponders. Low PDL2 and MDSC% levels were significantly associated with favorable mutations (NPM1, t(8;21)), whereas high levels correlated with FLT3-ITD and poor cytogenetic features. Conclusion Elevated PDL2 expression and MDSC percentages are associated with poor treatment response and adverse genetic risk in newly diagnosed AML patients. These markers show excellent predictive value and may serve as potential immunological biomarkers for treatment stratification and prognostication in AML.