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 f ragmentation into oligonucleosomal subunits. This requires macromolecu lar synthesis and is inhibited by interleukins (ILs). We performed exp eriments to analyse the possible effect of GCH on more differentiated lymphocytes, i.e. peripheral (from lymph nodes and spleen) T-lymphocyt es. The results show that in vitro dexamethasone (DEX) induces DNA fra gmentation and cell death not only in thymocytes but also in mature T cells. We also tested the possible role of interleukins (ILs) in the m odulation 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 cor relates with induction of c-jun (a component of AP-1 transcription fac tor). Furthermore high doses of IL-2 are able to induce apoptosis in b oth thymocytes and peripheral T cells. These data indicate that both t hymocytes and peripheral T cells undergo apoptosis in response to appr opriate stimuli and suggest that GCH and ILs interact in regulating T- lymphocytes apoptotic death.