Fig. 4

Reactivity of NK cells following surface coating. A Quantification of IFN-γ secretion from NK Cells and HALipid-NK cells. A positive control group was established, wherein NK cells were exposed to lipopolysaccharide (LPS) to stimulate an inflammatory response associated with IFN-γ secretion. The secreted IFN-γ was quantified by ELISA. (*) indicates a significant difference compared to NK cells and HADS-NK cells (p < 0.05). B Availability of native ligands on HALipid-NK cells. Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) and Fas ligand (FasL) were selected as essential ligands on NK cells for cancer recognition. NK cells were treated with APC-conjugated TRAIL and FasL antibodies immediately after coating. Fluorescence signals of antibodies were detected using flow cytometry. (*) indicates a significant difference compared to NK cells and HADS-NK cells (p < 0.05) (C) Schematic illustration of the internalization of coating materials (specifically, both HA-PEG-DMPE and HA-PEG-Chol) anchored on the NK cell surface. D Proliferation of NK cells coated with a 1 mg/mL of HA-PEG-Lipid solution. Proliferation levels were measured at 0, 24, and 48 h by CellTiter-Blue assay. (*) indicates a significant difference compared to NK cells, HADS-NK cells, and HADM-NK cells (p < 0.05) at the same time point. (n.s.) indicates no statistically significant difference between experimental groups