IL33 and Sepsis: Moreover, Nascimento’s results showed that endogenous IL-33, released during sepsis, induces the switch of macrophages toward M2 polarization, which has an essential function in the expansion of the Treg cell population via the production of IL-10 [33]; another study found that exogenous IL-33 resulted in the expansion of TIGIT+ Tregs depending on the STAT6 and M2 macrophages, contributing to the development of long-term sepsis-induced immunosuppression [61].