Retinoic acid regulates IgG Fc receptor expression in human myelomonocytic leukemia cells and normal peripheral monocytes

The regulation of IgG Fc receptor (FcγR) expression by retinoic acid (RA) in human myelomonocytic cells at different stages of maturation was studied. RA suppressed IgG‐coated erythrocyte (EA) rosette formation of myelomonocytic cells blocked at relatively late stages of differentiation such as ML‐1, U‐937, THP‐1‐T, normal monocytes, and fresh cells of patients with acute myelomonocytic leukemia. However, RA increased the percentage of EA rosetting promyelocytes of HL‐60 and of patients with acute promyelocytic leukemia and a part of myeloblasts isolated from acute myelogenous leukemia patients. Other myeloblasts including KG‐1a, KG‐1, and fresh cells from patients with acute myelogenous leukemia were not affected. A kinetic study using HL‐60 and THP‐1‐T demonstrated that an increase required at least a 48‐h exposure and that the maximum decrease required approximately 6 h. The RA effect on both cell lines was dose‐dependent. The number of FcγR of HL‐60 and THP‐1‐T treated with RA became very close, although untreated THP‐1 had almost 10 times as many as HL‐60. Kd for IgG in both THP‐1‐T and HL‐60, either untreated or treated with RA, remained unchanged. These observations indicate that one of the important roles of RA is regulation of FcyR expression in myeloid cells.