Development of the cell contact-mediated accessory function for T-cell proliferation in a human promyelocytic leukaemia cell line, HL-60, by 1,25-dihydroxyvitamin D3

• Published in: Immunology 1992-04, Vol.75 (4), p.619-625
• Main Authors: SHINBORI, T, YAMADA, M, KAKIMOTO, K, ARAKI, S, ONOUE, K
• Format: Article
• Language: English
• Subjects: Analysis of the immune response. Humoral and cellular immunity; Antigen-Presenting Cells - immunology; Biological and medical sciences; Calcitriol - immunology; Cell Adhesion Molecules - analysis; Cell Communication - immunology; Cell Division - immunology; Cell interactions; Cell Line; Dose-Response Relationship, Immunologic; Fundamental and applied biological sciences. Psychology; Fundamental immunology; HLA-DR Antigens - analysis; Humans; Immunobiology; Intercellular Adhesion Molecule-1; Interferon-gamma - immunology; Kinetics; Leukemia, Promyelocytic, Acute - immunology; Lymphocyte Activation - immunology; Monocytes - immunology; Recombinant Proteins; T-Lymphocytes - immunology
• ISSN: 0019-2805; 1365-2567

A human promyelocytic leukaemia cell line, HL-60 cells, did not show accessory cell (AC) function to potentiate the proliferation of human T cells induced by anti-CD3 antibody coupled to latex beads (alpha T3-L). This was found to be at least due to the inability of HL-60 cells to express certain molecules which are inducible with interferon-gamma (IFN-gamma) on mature monocytes and are necessary for interaction with T cells. HL-60 cells acquired the ability to express such surface molecules by stimulation with IFN-gamma when the cells were pretreated with 1,25-dihydroxyvitamin D3 (Vit D). The effect of Vit D was reversible, that is, the AC function of the HL-60 cells was lost when the cells were cultured in Vit D-free medium for 7 days. It was also found that HL-60 cells treated with IFN-gamma and then with Vit D did not show significant AC function. The flow cytometric analysis showed that the expression of HLA-DR and intercellular adhesion molecule-1 (ICAM-1) was highly increased on HL-60 cells when stimulated with IFN-gamma after treatment with Vit D. The expression of ICAM-1 was also induced with IFN-gamma on untreated cells but in lower amounts. Monoclonal antibodies against ICAM-1 and HLA-DR inhibited the alpha T3-L-induced T-cell proliferation, indicating that these molecules are at least required for contact-mediated AC function. Thus our study revealed that HL-60 cells express cell surface interaction molecules necessary for potentiating the T-cell proliferation through two steps, differentiation with Vit D to mature monocyte-like cells followed by stimulation with IFN-gamma.