IL1B and viral myocarditis: Rivadeneyra et al. reported that human neutrophils internalized and recognized CVB3 through endosomal TLR8 and then triggered NF-κB signalling, resulting in the upregulation of CD11b, strengthening of the adhesion to fibrinogen and fibronectin, and increase in secretion of IL-6, IL-1β, TNF-α, and IL-8, which suggests that neutrophils inhibit viral myocarditis development through TLR8 [49].