Hydrocortisone (50 nM) shows a dose-dependent down-regulation of GR transcript in hCMEC/D3 cells. Hydrocortisone supplementation of the serum-reduced cell differentiation medium leads to a significant increase in TER across the hCMEC/D3 monolayer^[1]. Hydrocortisone-treated Dendritic cells (DCs) show a decreased expression of MHC II molecules, the costimulatory molecule CD86, and the DC-specific marker CD83, as well as a strongly reduced IL-12 secretion. Hydrocortisone-treated DCs inhibit production of IFN-γ but induce an increased release of IL-4 and no change in IL-5^[2]. Hydrocortisone reduces postischemic oxidative stress, perfusion pressure, and transudate formation. Hydrocortisone inhibits postischemic shedding of syndecan-1, heparan sulfate, and hyaluronan as is release of histamine from resident mast cells^[3].