Analysis of susceptibility of mature human T lymphocytes to dexamethasone‐induced apoptosis

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Abstract
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.