Fig. 4: IL-2 treatment could rescue the phenotypes of Trim28 deficiency.

a Naive CD8⁺ T cells from WT and Trim28^-/- mice were cultured under anti-CD3/28 stimulation for 3 days. Expression of IL-2 was analyzed by flow cytometry. b Naive CD8⁺ T cells from WT and Trim28^-/- mice were cultured with or without IL-2 under anti-CD3/28 stimulation for 3 days. Representative FACS plot showing IFN-γ expression. c Trim28^fl/flCd8a^Cre mice and their littermate Trim28^fl/fl mice were infected with LCMV Armstrong virus. IL-2 production by antigen-specific CD8⁺ T cells in spleens was measured. d LCMV Armstrong infected-Trim28^fl/flCd8a^Cre mice and their littermate Trim28^fl/fl mice were intraperitoneally injected with or without mIL-2 (10 μg per mouse) every two days starting from day 1. Expression of IFN-γ by antigen-specific CD8⁺ T cells in different groups was measured. e–i Naive CD8⁺ T cells from WT and Trim28^-/- mice were cultured with or without anti-IL-2 under anti-CD3/28 stimulation for 3 days. RNA-seq was conducted after a 3-day culture. e Volcano plot shows transcriptome differences between untreated and anti-IL-2 treated activated CD8⁺ T cells. f Genes regulated by anti-IL-2 treatment were extracted followed by analysis of and top enriched pathways. g Heatmaps illustrating the relative expression of T cell activation signature genes in untreated and anti-IL-2 treated activated CD8⁺ T cells. h Venn plot of overlapped genes which were upregulated and downregulated by Trim28^-/- activated CD8⁺ T cells and anti-IL-2 treated activated CD8⁺ T cells. i GSEA enrichment of signature genes regulated by anti-IL-2 treatment in the transcriptome of CD8⁺ T cells from Trim28^fl/flCd8a^Cre mice. Each dot represents one individual replicate (n = 3 per group in (a, b). Each dot represents one individual mouse (n = 5 per group in c, n = 4 per group in (d). Statistical significance was tested by unpaired two-sided Student’s t-test (a–d). Data are representative of two (c, d) and three (a, b) independent experiments.