Role of NLRP3, IL-18, and IL-18R signaling for exhaustion mechanisms in the interaction of myeloid cells and CD8+T cells

Background Infiltration of CD8+cytotoxic T-cells (CTL) in pancreatic ductal adenocarcinoma (PDAC) is an important factor in determining prognosis. Recently, we have shown that IL-18 receptor (IL-18R) signaling induces a dysfunctional state of intratumoral cytotoxic CD8+T cells, resulting in the loss of effector function and specific changes in the transcriptional profile. The NLRP3 inflammasome complex activates IL-18 and is commonly expressed in macrophages.