Alum and antigen are phagocytosed by an APC and, through an unknown mechanism, activate the Nlrp3 inflammasome, resulting in secretion of the pro-inflammatory cytokines IL-1β, IL-18 and IL-33 and potentially other immune modulatory molecules. In conjunction with antigen recognition on the APC by the T-cell receptor (TCR), IL-1 receptor (IL-1R) stimulation (or another inflammasome-dependent signal) provides ‘signal 2’ for CD4+ T-cell priming, the first step in generation of adaptive immunity.