Figure 6

Autophagy regulates PD-L1 expression in macrophages and in TAMs. (A) RT-PCR analysis of PD-L1 mRNA in peritoneal macrophages isolated from WT or ATG5^Mye−/− mice. (B) RT-PCR analysis of PD-L1 mRNA in RAW264.7 cells in the presence or absence of 100 nM bafilomycin A, 100 nM rapamycin or 30 µM resveratrol. (C) RT-PCR analysis of PD-L1 mRNA in peritoneal macrophages exposed to the conditioned medium of Hepa1-6 cells (CMH) or to control medium (CM) in the presence or absence of 100 nM bafilomycin A, 100 nM rapamycin or 30 µM resveratrol. (D) Representative images of PD-L1 (red), F4/80 (green) and Dapi (blue) labeling in peritoneal macrophages exposed to control medium (CM) or to the conditioned medium of Hepa1-6 cells (CMH) in the presence or absence of 100 nM bafilomycin A, 100 nM rapamycin or 30 µM resveratrol (original magnification × 400). (E) RT-PCR analysis of iNOS, CCL3, Clec7A and Mgl1 mRNA in peritoneal macrophages in the presence or absence of 100 nM bafilomycin A, 100 nM rapamycin or 30 µM resveratrol. Data are shown as mean ± SEM of 6 samples per condition. ^&p < 0.05 for WT vs ATG5^−/−, *p < 0.05 for treatment vs control, ^Δp < 0.05 for CMH vs CM, ^∇p < 0.05 for CMH vs CMH + bafilomycin A or CMH + rapamycin or CMH + resveratrol.