Studies have shown that during P. brasiliensis infection, NLRC4 inhibits Prostaglandin E2 production, which is required for NLRP3-inflammasome-triggered IL-1β at the early phase of infection, while in the later phase of infection reduces IL-18 levels, abrogates CD8+IFN-γ+T cell responses, and promotes uncontrolled fungal growth (134). This evidence concerns the gene CD8A and infection.