Plasma Level of Programmed Death Receptor Ligand-1 and CD25 in Chronic Myeloid Leukemia Patients and their Correlations with Response to First-Line Therapy

Abstract

Background: Chronic myeloid leukemia (CML) is a clonal myeloproliferative neoplasm that is characterized by the presence of the Philadelphia (Ph) chromosome, which results from a reciprocal translocation between the breakpoint cluster region (BCR) of chromosome 22 and the Abelson homolog 1 (ABL1) region of chromosome 9. Programmed death-ligand 1 (PD-L1; also known as B7 homolog 1 and CD274) is an immune checkpoint protein, and its engagement with programmed cell death protein-1 (PD-1) receptor on T cells activates co-inhibitory signaling to suppress the function of cytotoxic T lymphocytes (CTLs). Interleukin-2 receptor (IL-2R, CD25) expression is a soluble form of the a-chain of IL-2R (sIL-2R). The IL-2/IL-2 receptor α (IL-2RA) signaling pathway is essential for the regulation of immune responses. Objective: To assess the plasma level of PDL-1 and CD25 in patients with CML and their correlations with response to the first line of therapy, tyrosine kinase inhibitor (imatinib). Materials and Methods: This case-control study was conducted on 66 patients with CML in the chronic phase (CP) from May 2019 to October 2019. The patients were sequentially selected and subdivided into three subgroups: 20 new diagnoses before starting treatment, 30 imatinib therapy responders, and 16 imatinib resistant for each group. Plasma samples were tested for the levels of PD-L1 and CD25 by the enzyme-linked immunosorbent assay technique. Results: Programmed cell death ligands were significantly increased in the plasma of patients with CML compared with the control group, and there was a significant increase in the plasma PD-L1 of patients with a new diagnosis compared with imatinib responders and patients who were resistant. There was no significant difference in PD-L1 level between the responder and resistant groups. Soluble CD25 was significantly increased in the plasma of patients with CML compared with the control group, and there was a significant increase in the plasma CD25 of patients with a new diagnosis compared with imatinib responders and patients who were resistant. There was no significant difference in CD25 level between responder and resistant groups. Conclusion: Plasma PD-L1 and CD25 levels were significantly higher in adult patients with CML compared with healthy subjects, and these levels were significantly higher in patients with CML who are newly diagnosed compared with imatinib therapy responders and resistant counterparts. There is no significant difference between responders and resistant groups in regard to PD-L1 and CD25.