The involvement of the glucocorticoid receptor (GR) in cAMP-induced apoptosis in a GR-deficient derivative of the CEM.C7 human T-ALL line was investigated. Incubation of the parental CEM.C7 cells with agents that elevate cAMP levels (dibutyryl cAMP and forskolin) resulted in DNA fragmentation characteristic of apoptotic cell death, whereas the GR- deficient ICR.27 cells were insensitive to the cytolytic effects of cAMP. Reconstitution of GR expression by transfection not only restored glucocorticoid sensitivity to the ICR.27 cells, but also promoted sensitivity to induction of apoptosis by cAMP. Thus, cAMP-induced apoptosis in T cells appears to occur via ligand-independent stimulation of at least some aspects of glucocorticoid receptor function.
|Original language||English (US)|
|Number of pages||4|
|Journal||Journal of Immunology|
|State||Published - 1995|
ASJC Scopus subject areas
- Immunology and Allergy