Fig. 4: MHC-I blockade restores NK cell-mediated ADCC activity against malignant T cells in MF skin lesions.

a MHC-I blockade restored ADCC activity of autologous NK cells against malignant T cells in MF tumor skin lesions (N = 4) when cell-surface receptor-specific targeted mAb (CD52-mAb) was used as an opsonizing agent. Data were presented as mean values +/– SEM. The p values were calculated using unpaired, one-way ANOVA test. b, MHC-I blockade resulted in ADCC cluster formation, showing that opsonized malignant T cells from tumor skin lesions were surrounded by autologous NK cells. NK cells and T cells were labeled with CFSE and Far Red, respectively. Scale bar = 50 µm. c, The corresponding ADCC activity from each group of cells in (b), demonstrating restored NK cell-mediated ADCC activity against malignant T cells in MF skin lesions upon MHC-I blockade. N = 4 in group I; N = 5 in group II; N = 6 in group III; N = 6 in group IV; N = 2 in group V; N = 6 in group VI. Data were presented as mean values +/– SEM. The p values were calculated using unpaired, two-tailed student’s t test. n.s., not significant. d FACS analysis revealed KIR blockade enhanced ADCC activity of autologous NK cells against malignant T cells from MF skin lesions when anti-CD52-mAb or anti-CCR4-mAb was used as the opsonizing agent. e, Flow cytometrical detection showed enhanced ADCC against skin tumor T cells when KIR was blocked (N = 7). Data were presented as mean values +/– SEM. The p values were calculated using paired, two-tailed student’s t test. f LDH release detection showed increased ADCC against skin tumor T cells when KIR was blocked (N = 7). Data were presented as mean values +/– SEM. The p values were calculated using paired, two-tailed student’s t test. Source data are provided as a Source Data file.