Fig. 1

Mechanisms of exosome regulation of immunity in sepsis. Exosomes derived from immune cells are instrumental in orchestrating a balance between immunoregulatory and autoimmune responses within a complex network of immune interactions. These vesicles are rich in bioactive molecules and play key roles in the inflammatory process by guiding PMN recruitment and migration, supporting the innate immune response, and influencing macrophage polarization towards either pro-inflammatory M1 or anti-inflammatory M2 states, thereby shaping the progression of inflammation. DC-derived exosomes are crucial in engaging memory T cells, triggering their differentiation into Th1, Th2, or Treg cells and fostering a proliferative response essential for robust immunity. Additionally, these exosomes enhance adaptive immunity by aiding in B cell maturation and improving antigen presentation. Simultaneously, they significantly impact the activation and proliferation of CD8⁺ T cells, highlighting their extensive involvement in modulating immune responses, particularly during sepsis. PMN neutrophil, DC dendritic cell, NET neutrophil extracellular traps, Th1 type 1 helper T cells, Th2 type 2 helper T cells, Ab antibody