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. 2023 Nov 2;7(1):13–27. doi: 10.1093/abt/tbad025

Figure 3.

Figure 3

h128-3-induced LILRB4 internalization in FcγR high monocytic AML is promoted by FcγRI crosslinking. (A) Measurement of the surface expression of LILRB4 and FcγRI on HEK293-T LILRB4/FcγRI OE (HEK293-T RB4/1A OE) cells by flow cytometry. (B) Baseline LILRB4 internalization induced by h128-3 in THP-1, Mono-mac-6 and HEK293T RB4/1A OE cells. Cells were treated with 1 μg/ml of h128-3 or irrelevant hIgG and cultured at 37°C for 24 h before measurement of LILRB4 expression by FACS (n = 3). (C–E) h128-3-induced internalization of LILRB4 in THP-1 (C), Mono-mac-6 (D) and HEK293T RB4/1A OE (E) cells blocked with 100-fold irrelevant hIgG (IVIg) prior to h128-3 treatment (n = 3). FcγRI on cells was nonspecifically blocked with 1% BSA (-IVIg) or 1% BSA and 100 μg/ml of IVIg (+IVIg) for 30 min at 37°C prior to treatment with 1 μg/ml of isotype control hIgG or h128-3 for 24 h at 37°C. LILRB4 internalization was measured by flow cytometry.