Extraordinarily elevated CD33 expression in CD56(+)CD3(–) cells in the bone marrow of a patient with relapsed acute myeloid leukemia: a case report

Based on genetic risk allogeneic stem cell transplantation (allo-SCT) is the only curative treatment for some forms of acute myeloid leukemia (AML). However, post-transplantation relapse remains a frequent cause of transplantation failure. Natural killer (NK) cells and CD8+ T cells are important effector lymphocytes with pivotal roles in tumor surveillance and anti-tumor immune response. In this study, a 14-year-old female patient with AML was treated with allogeneic peripheral blood stem cell transplantation (allo-PBSCT). Bone marrow relapse was found 6 months later. Thereafter, the patient was treated with DAE (daunorubicin, cytosine arabinoside, and etoposide), followed by IAE (idarubicin, cytosine arabinoside, and etoposide), and then MA (mitoxantrone and cytosine arabinoside) regimens. A series of experiments including Wright-Giemsa stain analyses, cytogenetic analysis and flow cytometry were conducted to investigate the characteristic of the patient. Although there was a short remission after the DAE regimen, the patient experienced another relapse after finishing the MA regimen. The CD56(+)CD3(‒) cells in the bone marrow showed severely impaired activation and anti-tumor function, while extraordinarily increased CD33 expression. Moreover, the proportion of multifunctional effector CD8(+) T cells remained stable, though they had high PD-1 expression. These findings revealed the dysfunction of abnormal CD56(+)CD3(–) cells with high CD33 expression, which might be targetable and related to the relapsed/refractory AML after allo-SCT.