Fcγ receptor-mediated biological activities of human leukemic cell lines and their modulation by transforming growth factor-β1 and interleukin 6

• Published in: Cytokine (Philadelphia, Pa.) Vol. 5; no. 3; pp. 255 - 263
• Main Authors: Morikawa, Minoru, Harada, Naoki, Nunomura, Yuka, Koike, Tsuneaki, Hashimoto, Seiji, Soma, Gen-ichiro, Yoshida, Takeshi
• Format: Journal Article
• Language: English
• Published: Elsevier Ltd 1993
• Subjects: active oxygen molecules; ADCC; Fcγ receptor; human leukemic cell lines; IL-6; TGF-β1; Fcγ receptor; TGF-β1; active oxygen molecules; human leukemic cell lines; ADCC; IL-6
• ISSN: 1043-4666; 1096-0023
• DOI: 10.1016/1043-4666(93)90013-U

Previously we reported that transforming growth factor-β1 (TGF-β1) remarkably enhanced the differentiation of human leukemic cell lines, HL-60 and THP-1, in the presence of 1α,25-dihydroxyvitamin D 3 (VD 3) and also that it induced Fc receptor for immunoglobulin G (FcγR), type IIIB, in the presence of retinoic acid (RA). The present study revealed that TGF-β1 enhanced the FcγRI- and FcγRII-mediated antibody-dependent cellular cytotoxicity (ADCC) of the cells differentiated in the presence of VD 3 and RA. However, production of active oxygen molecules was suppressed by TGF-β1. On the other hand, IL-6 stimulated production of active oxygen molecules and ADCC of the cells treated with VD 3 and tumor necrosis factor-α (TNF-α). Furthermore, the levels of cell surface FcγRI and FcγRII were not clearly correlated with the ADCC. The TGF-β1 VD 3-treated HL-60 cells were able to synthesize mRNAs for TGF-β1 and TNF-α, although TNF-α protein was not detectable. These results suggest that TGF-β1 has a bifunctional role, either stimulatory or inhibitory, in the modulation of macrophage activities through FcγRs and that IL-6 stimulates certain macrophage activities in mature cells.