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. 2023 Oct 30;12(1):7–16. doi: 10.1158/2326-6066.CIR-23-0321

Figure 2.

Figure 2. Mechanisms of immune stimulation (A) and immunosuppression (B) mediated by secretomes emitted from dying cancer cells. Several types of cancer cell death result in the surface expression of calreticulin and/or the emission of danger signals (ATP and HMGB1), cytokines and chemokines. In a concerted approach, all these molecules activate antitumor immune responses, mediated by DCs priming T cells to become cytotoxic against tumors expressing cognate antigens. In addition, the NKp46 receptor of NK cells can directly recognize calreticulin on the surface of stressed cells to engage in tumor cell killing. Immunostimulatory secretomes are also essential for T-cell activation and trafficking into malignant lesions. In some cancers, cell death can attract immunosuppressive B cells and MDSCs, thereby contributing to tumor progression.

Mechanisms of immune stimulation (A) and immunosuppression (B) mediated by secretomes emitted from dying cancer cells. Several types of cancer cell death result in the surface expression of calreticulin and/or the emission of danger signals (ATP and HMGB1), cytokines and chemokines. In a concerted approach, all these molecules activate antitumor immune responses, mediated by DCs priming T cells to become cytotoxic against tumors expressing cognate antigens. In addition, the NKp46 receptor of NK cells can directly recognize calreticulin on the surface of stressed cells to engage in tumor cell killing. Immunostimulatory secretomes are also essential for T-cell activation and trafficking into malignant lesions. In some cancers, cell death can attract immunosuppressive B cells and MDSCs, thereby contributing to tumor progression.