Abstract
Interleukin-1β (IL-1β) can limit tumor growth by promoting T cell-mediated antitumor immune responses. Several chemotherapeutic agents can stimulate the production of IL-1β by tumor-infiltrating leukocytes via the NLRP3 inflammasome. We have recently demonstrated that some chemotherapeutics can also trigger the secretion of IL-1β by driving the assembly of the caspase-8- and FADD-containing platform known as the ripoptosome.