Since there is no expression of IL-38 in mouse CD4+ T cells, but mouse CD4+ T cells display surface expression of IL-36R (IL-38 specific receptor) [10, 11], making them capable of receiving the biological signal of IL-38 released by a large number of infiltrated immune cells (e.g., B cells, NK cells, macrophages, and DCs) during the acute phase of infection, this may be an important mechanism by which Anti-IL-38 Abs participate in the regulation of Th cells differentiation in vivo. Here, IL1RL2 is linked to infection.