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. 2021 Sep 6;19:268. doi: 10.1186/s12951-021-01017-w

Fig. 6.

Fig. 6

PD-L1 blockade by BMS-1 enhanced Nano-DOX-stimulated M1-like activation of TAMs. AC BMS-1 promoted Nano-DOX-induced surface markers (CD80, CD86 & MHC-II) of M1-like activation in hM2 in the presence of A549 cells. DF BMS-1 promoted Nano-DOX-induced surface makers (CD80, CD86 & MHC-II) of M1-like activation of mM2 both in the presence and absence of Lewis cells. G, H BMS-1 promoted Nano-DOX-induced phagocytosis of fluorescent latex beads by hM2 and mM2 both in the presence and absence of the cancer cells. I, J BMS-1 promoted Nano-DOX-induced GBP5 in single-cultured hM2 and mM2. Cell surface CD80, CD86 & MHC-II were assayed by FACS analysis of immunofluorescent staining and GBP5 protein was assayed by western blotting. K Nano-DOX treatment led to increased immunohistological staining of CD80, CD86, MHC-II and GBP5 in subcutaneous xenografts of Lewis cells in mice. FACS histogram geometric means were used to quantify mean fluorescence intensity (MFI). Values were means ± SD (n = 3, *p < 0.05). Drug concentration was 2 μg/mL for DOX and Nano-DOX and 1 μM for BMS-1 in the in vitro experiments and treatment duration was 24 h. Representative FACS dot plots for A-H were provided in Additional file 1: Figure S6