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Fig. 2 | Journal of Experimental & Clinical Cancer Research

Fig. 2

From: Pyroptosis at the forefront of anticancer immunity

Fig. 2

Pyroptosis heats anticancer immunity. ‘Cold tumor’: tumor cells create an immune tolerant microenvironment and avoid immune detection and killing by recruiting immunosuppressive cells, increasing immune checkpoint proteins, impeding antigen presentation, and releasing immune inhibitory factors. ‘Warming tumor’: various strategies are used to induce tumor cell pyroptosis and “heat” tumors from immune-silent states. ‘Warm tumor’: pyroptotic tumor cells release pro-inflammatory cytokines and immunogenic material that prompt immune cell activation and recruitment. ‘Hot tumor’: infiltrated immune cells recognize and kill tumor cells, and this killing may participate in a positive feedback loop that enhances tumor-specific immunity. Tumor elimination may be further increased through combinatorial therapeutic strategies. CAR-T, chimeric antigen receptor T cell; CCCR-NK, chimeric costimulatory converting receptor natural killer cell; DC, dendritic cell; GSDMs, gasdermin proteins; HMGB1, high-mobility group box protein 1; IFN-γ, interferon-gamma; IL, interleukin; MDSCs, myeloid-derived suppressor cells; MHC, major histocompatibility complex; NK, natural killer cell; NP, nanoparticle; PD-L1, programmed death-ligand 1; PD-1, programmed cell death protein 1; TNF-α, tumor necrosis factor-alpha; Tregs, regulatory T cells

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