Fig. 1

Inflammasome components and functions. After sensing specific stimuli, for example through NEK7, a member of the family of mammalian NIMA-related kinases (NEK proteins),the sensor NLR family pyrin domain containing 3 (NLRP3) assembles together with the adaptor apoptosis-associated speck-like protein (ASC) and the effector pro-caspase-1, via homotypic interactions between the N-terminal pyrin domain (PYD) domain of NLRP3 and the PYD domain of ASC, as well as between the respective Caspase Recruitment Domains (CARD) of ASC and pro-caspase-1. Assembly of the NLRP3 inflammasome leads to activation of caspase-1 (CASP1), which then cleaves the pro-forms of interleukin-1beta (IL-1β) and -18(IL-18), resulting in the secretion of biologically active cytokines, as well as gasdermin D (GSDMD), resulting in pyroptosis via the formation of pores at the plasma membrane. Inflammasomes are activated through different mechanisms and release IL-1β and IL-18 to initiate inflammation. In the figure we show all the cells like regulatory T cells (TREG), monocytes, stromal cells, natural killer (NK) cells, myeloid-derived suppressor cells (MDSC), macrophages, tumor cells, cancer-associated fibroblasts (CAF), tumor-associated macrophages (TAMS) and dendritic cells (DC) cells, able to release cytokines and chemokines such as IL-6 (interleukin 6), IL-8 (interleukin 8), IL-10 (interleukin 10), transforming growth factor-b (TGF-b), tumor necrosis factor-a (TNF-a) and C–C motif chemokine ligand 2 (CCL2). In details, cancerous cells and stromal cells can release chemokines and lead to neutrophil infiltration. Neutrophils will in turn secret more pro-inflammatory cytokines including interleukins and interferons. B cells and antibodies are also observable. TREG, TAMs, and MDSCs work together to enhance immunosuppression. The alteration of proinflammatory cytokines will lead to abnormal polarization of T helper cells