Fig. 4

Inflammasomes mediate the dynamic interplay between innate and adaptive immunity, shaping immune responses. A Inflammasomes in antigen-presenting cells (APCs) release IL-1 family cytokines and HMGB1, which have a significant impact on T cell immune responses. The arrows in the figure are color-coded to match the font color of the effects they represent. Activation of inflammasomes can also trigger the expression of specific genes in innate immune cells, thereby influencing adaptive immunity. For instance, in macrophages, the AIM2 inflammasome is activated upon recognition of phagocytosed tumor DNA following antibody-dependent cellular phagocytosis (ADCP). This activation leads to the upregulation of IDO and PD-L1, resulting in T cell immunosuppression. Additionally, a deficiency of Tim-3 in dendritic cells (DCs) causes an accumulation of reactive oxygen species (ROS) and subsequent activation of the NLRP3 inflammasome, which enhances the stemness and effector functions of CD8⁺ T cells. B Cytokines produced by T cells can modulate the activation or inhibition of inflammasomes in APCs. T cells that secrete perforin and TNF-α can activate the NLRP3 inflammasome, while cytokines like IL-10 and IFN-γ inhibit its assembly. Moreover, the activation of CD8⁺ T cells in response to anti-PD-1 therapy initiates a PD-L1/NLRP3 inflammasome signaling cascade. This cascade ultimately leads to the recruitment of polymorphonuclear myeloid-derived suppressor cells (PMN-MDSCs) into tumor tissues, providing negative feedback that inhibits CD8⁺ T cell activation and anti-tumor immune responses