Modulation of the expression of CD4 on HL-60 cells by exposure to 1,25-dihydroxyvitamin D3.
The CD4 molecule functions as a receptor for the binding and infectivity of the human immunodeficiency virus (HIV). It is of interest, therefore, to develop procedures for its down-regulation. In the present study, the effect of 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) on the expression of cell surface antigens of the HL-60 promyelocytic leukemia cell line was analyzed. Exposure of HL-60 cells to 1,25(OH)2D3 resulted in down-regulation of CD4 as assessed by their staining with the Leu-3a monoclonal antibody (MoAb). This treatment increased the staining of HL-60 cells with the monocyte-specific 63D3 MoAb. In contrast to the rapid elimination of cell surface CD4 by exposure of HL-60 to phorbol myristate acetate (PMA), the maximal reduction of CD4 by 1,25(OH)2D3 was attained within 48 h after the beginning of the exposure.
Schlesinger
M
M
Hubert H. Humphrey Center for Experimental Medicine and Cancer Research, Hebrew University, Hadassah Medical School, Jerusalem, Israel.
Bar-Shavit
Z
Z
Hadar
R
R
Rabinowitz
R
R
D000911:Antibodies, Monoclonal; D015704:CD4 Antigens / Q000096:biosynthesis*; D002117:Calcitriol / Q000494:pharmacology*; D005455:Fluorescent Antibody Technique; D007700:Kinetics; D007963:Leukocytes, Mononuclear / Q000187:drug effects* / Q000276:immunology; D013755:Tetradecanoylphorbol Acetate / Q000494:pharmacology; D014407:Tumor Cells, Cultured
D000911:Antibodies, Monoclonal; D015704:CD4 Antigens; D002117:Calcitriol; D013755:Tetradecanoylphorbol Acetate