Fig. 5. TRIM21 deficiency potentiates radiation-induced antigen presentation.

a, b WT and TRIM21-KO NPC cells were treated with or without IR. After 48 h, the mRNA expression of antigen presentation molecules, including HLA-A, B2M, TAP1 and TAP2, was measured by qPCR (a), and the surface MHC-I molecules HLA-A/B/C and β2m were analysed by flow cytometry (b). The results are representative of three independent experiments. c A total of 1 × 10⁶ WT or TRIM21-KO SUNE1 cells were subcutaneously injected into the flanks of BALB/c nude mice, and 1 × 10⁶ WT or TRIM21^−/− MC38 cells were subcutaneously injected into the flanks of C57BL/6 mice. Tumour formation was confirmed 10 days later, and the SUNE1 and MC38 tumours in mice in the IR-treated groups were then subjected to focal radiation with a single fraction of 6 Gy or 15 Gy, respectively. Tumours were dissected 3 or 5 days after IR. The expression of antigen presentation molecules, including HLA-A, B2M, TAP1 and TAP2 in SUNE1 tumours (d, n = 4) and B2m, Erap1, Tapbp, Tap1 and Tap2 in MC38 tumours (e, n = 4), was measured by RT–qPCR, and surface MHC-I molecules on murine CD45^– cells in SUNE1 tumours (f, n = 5) and MC38 tumours (g, n = 3) were analysed by flow cytometry. h, i qPCR analysis of IFNB1, CCL5 and CXCL10 mRNA expression in SUNE1 tumours (h, n = 4) and MC38 tumours (i, n = 4) as indicated in (c). All data are presented as the mean ± SEM. Statistical analysis was performed by one-way ANOVA with Tukey’s test for multiple comparisons (a, b and d–i).