Analysis of susceptibility of mature human T lymphocytes to dexamethasone-induced apoptosis.
We present evidence that dexamethasone (Dex), a synthetic glucocorticosteroid, causes apoptosis in mature human T cells, similarly to what has been reported for murine T lymphocytes. Human T cell clones and short-term activated T lymphocytes treated with Dex show the characteristic pattern of apoptotic cells, such as hypodiploid nuclei, chromatin condensation and DNA fragmentation into oligonucleosomal fragments. However, Dex susceptibility of T cells to apoptosis is cell cycle-dependent. The progression in the proliferative cell cycle (G1 versus S) rescues Dex-treated T cells from apoptosis. Moreover, occupancy of the T cell receptor reverses Dex-induced apoptotic phenomena. These observations suggest that glucocorticoids contribute to the regulation of the proliferative or the suicidal response of antigen-activated human T cells.
Tuosto
L
L
Department of Cellular and Developmental Biology, University La Sapienza, Rome, Italy.
Cundari
E
E
Gilardini Montani
M S
MS
Piccolella
E
E
D000818:Animals; D017209:Apoptosis / Q000187:drug effects* / Q000502:physiology; D002453:Cell Cycle / Q000502:physiology*; D002478:Cells, Cultured; D004247:DNA / Q000032:analysis; D003907:Dexamethasone / Q000494:pharmacology*; D004587:Electrophoresis, Agar Gel; D005434:Flow Cytometry; D006801:Humans; D007739:L Cells; D008213:Lymphocyte Activation / Q000187:drug effects; D051379:Mice; D011948:Receptors, Antigen, T-Cell; D013601:T-Lymphocytes / Q000187:drug effects*
D011948:Receptors, Antigen, T-Cell; D003907:Dexamethasone; D004247:DNA