Fig. 5

HCQ induces CD8⁺ T cell-based tumour suppression via macrophages. a Lewis-bearing C57BL/6 J mice (n = 5) were instilled with HCQ and/or i.v. followed by i.v. DOX treatment in the presence or absence of clodronate liposomes. On day 24, the mice were sacrificed for lung weight evaluation. b Lewis-bearing C57BL/6 J mice (n = 5) were instilled with HCQ and/or followed with i.v. DOX treatment in the presence or absence of anti-CCL2 antibody. On day 24, the mice were sacrificed for lung weight evaluation. c Tumour-infiltrating leukocytes (TILs) were isolated from (a), and the proportion of CD3⁺CD8⁺ T cell among TILs was analysed by flow cytometry (n = 3). d Tumour-derived CD8⁺ T cell were sorted from PBS- and HCQ-treated Lewis-bearing mice with or without additional DOX treatment and cultured with IL-2 or IL-2 + CD3/CD28 beads. The data were quantified by calculating the T cell number at day 3 compared with that at day 0 (n = 3). e The mRNA expression of Ifng, Tgfb1 and IL10 was analysed in tumour-derived CD8⁺ T cell, which were sorted from PBS- and HCQ-treated Lewis-bearing mice with or without additional DOX treatment (n = 3). f and g The mRNA expression of Ifng, IL12b, IL1b, IL6, Tgfb1, IL10 and Vegfa was analysed in tumour tissue from PBS- and HCQ-treated Lewis-bearing mice in the presence or absence of DOX (n = 3). For all graphs, the error bars indicate the mean ± s.e.m., *P < 0.05; **P < 0.01; ***P < 0.001; ns, no significant difference. The data shown are representative of three independent experiments