This harmful cascade of events is triggered by the innate sensing of both pathogen-associated molecular patterns and malaria damage-associated molecular patterns (PAMPs and DAMPs, respectively) by dendritic cells (DCs) and macrophages in the blood and lymphoid tissues, leading to an increased release of proinflammatory mediators, including interferon gamma (IFN-γ), tumour necrosis factor (TNF), interleukin-1 beta (IL-1β), and IL-6 [16] (Figure 2). Here, IL1B is linked to malaria.