Mechanisms of T-cell Apoptosis Induced by Glucocorticoids

Glucocorticoid effects on lymphoid cells depend on the cell type, the state of differentiation and the extracellular milieu. Cells often studied for glucocorticoid-dependent apoptosis include: rat and mouse thymocytes or splenocytes in vivo or in vitro; a variety of transformed lymphoid cell lines; lines of growth factor-dependent cells; and growth-stimulated peripheral blood lymphocytes. It is unwise to assume that all results in any one system are generally applicable. Only a moment's consideration of the diversity of lymphoid cells, and even of thymocytes themselves, shows that many states of differentiation define varying sensitivity to steroids. Such differences point out a valuable lesson: the apoptotic effects of glucocorticoids are influenced by a complex network of interactive signaling systems. Before we fully understand the apoptotic action of these steroids, it will be necessary to understand how these networks mesh. Each system has its merits and problems; the use of multiple systems has provided overlapping insights into the pathways involved in glucocorticoid-dependent lymphoid cell apoptosis. At times, visualization of the major shared themes is threatened by the inevitable contradictory data resulting from studying multiple systems, but in fact several common threads can be seen. In this light, this article briefly reviews recent developments in glucocorticoid-dependent lymphoid cell apoptosis.