Fig. 2. Mi-2β deficiency induced responses to immunotherapy in melanoma.

a A schematic for experimental strategy with anti-PD-1 treatment on genetically engineered melanoma mouse model. Mice carrying conditional alleles of Tyr::CreER;BRaf^CA;Pten^lox/lox or Tyr::CreER;BRaf^CA;Pten^lox/loxMi-2β^lox/lox were administered with tamoxifen for constant 5 days to activate CreER to cause melanocyte-specific conversion of Braf^CA to Braf^V600E, and the conversion of the Pten^lox/lox and Mi-2β^lox/lox alleles to null alleles, which expressed proteins of BRaf^V600E/Pten^null or BRaf^V600E/Pten^null /Mi-2β^null, respectively. Mice with measurable tumors were randomly treated with either control IgG (10 mg/kg) or anti-PD-1 (10 mg/kg) antibodies at day 9, 12, 15, 18 and 21 after Cre activation. b Survival of BRaf^V600E/Pten^null mice treated with IgG (n = 11) or anti-PD-1 (n = 12), and of BRaf^V600E/Pten^null /Mi-2β^null mice treated with IgG (n = 14) or anti-PD-1 (n = 11). Log-rank test was used for P value calculation, NS represents no significance. c TILs were assayed with flow cytometry. The number of CD8⁺ cells and CD4⁺ T cells gated within CD45⁺ T cells were demonstrated (n = 6). d Granzyme B expression in CD8⁺ T was determined and quantified by flow cytometry (n = 6). e Expression of activation markers on CD8⁺ T cells were determined by flow cytometry. MFI represents mean fluorescence intensity (n = 5). c, d, e Values represent mean ± SD. The unpaired, two tailed t-test. Source data are provided as a Source Data file.