Fig. 10

Schematic diagram showing how proBDNF dampens CD4⁺ T cell activity and contributes to the pathogenesis of SAE. In sepsis, proBDNF expression is increased in peripheral blood and meningeal immune cells, which then decreases the infiltration of CD4⁺ T cells in the meninges. As a result, meningeal pro-inflammatory cytokines such as IL-6 and IL-1β are upregulated, but anti-inflammatory cytokines including IL-4 and IL-13 are downregulated, finally leading to SAE. SAE, sepsis-associated encephalopathy