Fig. 6
From: Cortisol-induced immune suppression by a blockade of lymphocyte egress in traumatic brain injury
Schematic illustration of a possible mechanism underlying cortisol-mediated blockade of T cell egress. cAMP is one of the important second messengers downstream the S1P1 receptor and its production takes central part in the control of T cell egress. One of the cortisol (HC) activities may activate cAMP phosphodiesterase (PDE4) either directly or indirectly and enhance degradation of cAMP to 5′-AMP. Cortisol-facilitated degradation of cAMP may be one of the mechanisms where cortisol compromises T cell egress in the presence of S1P. On the contrary, rolipram inhibits PDE4, leading to increased levels of cAMP and promoting T cell egress