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. 2022 Jan 5;16:418–432. doi: 10.1016/j.bioactmat.2021.12.029

Fig. 3.

Fig. 3

In vitro immune cell death (ICD) induced by ROS generated from the Fenton-like reaction under the NIR II irradiation. (a) Schematic illustration of the DAMPs (CRT, ATP and HMGB1) released from the dying tumor cells to promote the DC mature, triggered by large amount of ROS generated from the degradation of H2O2 by CS-I/J@CM NPs under irradiation. (b) CLSM of CRT (red fluorescence) exposed on the cytomembrane (green fluorescence) of GL261 cells, after different treatment with or without CS-I/J@CM NPs (12.5 μg/mL) (scale bar: 20 μm). (c) Colocalization of CRT and cytomembrane of GL261 cells. (d) Flow cytometry analysis of CRT expose on GL261 cells after co-cultured with or without CS-I/J@CM NPs (12.5 μg/mL). (e) Detection of extracellular ATP secreted. (f) Detection of extracellular HMGB1 released. (g) Flow cytometry analysis of the maturation of DC (CD11c+CD80+CD86+). (h) Normalization of the maturation of DC in Fig. 3g. (*p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001, n = 5).