Dexamethasone and interleukins modulate apoptosis of murine thymocytes and peripheral T-lymphocytes

Glucocorticoid hormones (GCH) induce apoptotic cell death in immature thymocytes through an active process, characterized by extensive DNA fragmentation into oligonucleosomal subunits. This requires macromolecular synthesis and is inhibited by interleukins (ILs). We performed experiments to analyse the possible effect of GCH on more differentiated lymphocytes, i.e. peripheral (from lymph nodes and spleen) T-lymphocytes. The results show that in vitro dexamethasone (DEX) induces DNA fragmentation and cell death not only in thymocytes but also in mature T cells. We also tested the possible role of interleukins (ILs) in the modulation of apoptotic cell death. We show that DEX-induced apoptosis is inhibited by IL-2 and IL-4 and that the IL-4 induced inhibition correlates with induction of c-jun (a component of AP-1 transcription factor). Furthermore high doses of IL-2 are able to induce apoptosis in both thymocytes and peripheral T cells. These data indicate that both thymocytes and peripheral T cells undergo apoptosis in response to appropriate stimuli and suggest that GCH and ILs interact in regulating T-lymphocytes apoptotic death.