Antagonism of brain HMGB1 reversed the suppressed expressions of DC surface molecules, including CD80, CD86, and MHC-II, and improved T cell proliferation, cytokine secretion as well as the homeostasis of Th1/Th2 differentiation, suggesting that cerebral HMGB1 might also be responsible for sepsis-induced dysfunction of peripheral DCs. This evidence concerns the gene CD86 and Sepsis.