Practical limitations of monocyte subset repartitioning by multiparametric flow cytometry in chronic myelomonocytic leukemia

Monocyte subset repartitioning by multiparametric flow cytometry has recently been shown to be an effective tool in delineating patients with chronic myelomonocytic leukemia (CMML), from other reactive and clonal causes of monocytosis 1 , 2 , 3 . Based on the expression of CD14 and CD16, monocytes can be divided into three categories; CD14 + /CD16 − classical (MO1), CD14 low /CD16 + intermediate (MO2), and CD14 − /CD16 + non-classical monocytes (MO3), respectively 1 , 2 . These subsets differ in their chemokine receptor expression, phagocytic activity, gene promotor/enhancer profiles and have unique metabolic pathway dependencies 2 , 4 . It has also been shown that downregulation of hsa-miR-150 through methylation of lineage-specific promotors in CMML monocytes, results in impaired differentiation of MO1–MO3 monocytes, with TET3 being a potential target 5 .