The role of natural killer T cells in sepsis-associated acute kidney injury.

The condition of sepsis, defined by the misregulation of the body's defensive mechanisms against infection, culminates in the potential for catastrophic organ damage and stands as a primary driver of mortality in Intensive Care Units (ICU) settings. Among patients in a critical condition, sepsis is a predominant factor in the development of acute kidney injury (AKI), and the death rate among those with both sepsis and AKI is considerably higher, underscoring the importance of addressing this health crisis. Sepsis-associated acute kidney injury (S-AKI) is a complex process involving inflammation, microcirculatory issues, and metabolic disorders. Among these, the inflammatory response has become a focal point of interest. Bridging the innate and adaptive immunity, natural killer T (NKT) cells can be rapidly activated in sepsis, contributing to sepsis-associated injury and downstream activation of inflammatory cells through the emission of Th1 or Th2 cytokines. They also contribute to S-AKI through the TNF-α/FasL and perforin pathways. Alpha-Galactosylceramide (α-GalCer), acting as a powerful activator for type I NKT (iNKT) cells, is able to regulate the secretory profile of iNKT cells, responding to the pro-inflammatory response and immunosuppressive profiles of sepsis. This review examines the part played by NKT cells in S-AKI and whether α-Galcer could function as a significant regulator in sepsis, based on studies of regression-related mechanisms.