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Supplementary Figure S1. In vivo CRISPR screens to identify critical drivers of immune evasion; Supplementary Figure S2. Effects of Ripk2 depletion on tumor growth; Supplementary Figure S3. RIPK2 is overexpressed in human and mouse PDAC tissues; Supplementary Figure S4. Ablation of RIPK2 disrupts the desmoplastic TME; Supplementary Figure S5. RIPK2 modulates the immune profile and impairs anti-tumor T cell response; Supplementary Figure S6. RIPK2 restricts the activation and effector states of CD8+ T cells by impairing antigen presentation; Supplementary Figure S7. RIPK2 promotes MHC-I trafficking to lysosomes via NBR1; Supplementary Figure S8. RIPK2 ubiquitination promotes NBR1-mediated MHC-I degradation; Supplementary Figure S9. RIPK2 ablation potentiates the efficacy of PD-1 blockade; Supplementary Figure S10. Diagram illustrating RIPK2-mediated degradation of MHC I through autophagy–lysosome system.
Sang et al. (Thu,) studied this question.
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