Of note, IL-1β binds to its receptors on naïve T-cells and promotes Th1 and Th17 differentiation, leading to pro-inflammatory activities, whereas IL-18 counteracts IL-1β by preventing the Th17 response, Treg differentiation, and immune tolerance persistence, thereby balancing the control of infection [20,21,22]. The gene discussed is IL1B; the disease is infection.