Analysis of susceptibility of mature human T lymphocytes to dexamethasone-induced apoptosis
Autor: | E. Cundari, Enza Piccolella, M. S. Gilardini Montani, Loretta Tuosto |
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Rok vydání: | 1994 |
Předmět: |
endocrine system
medicine.medical_specialty T-Lymphocytes T cell Immunology Receptors Antigen T-Cell Apoptosis Biology Lymphocyte Activation Dexamethasone TCIRG1 Mice Interleukin 21 L Cells Internal medicine polycyclic compounds medicine Animals Humans Immunology and Allergy Cytotoxic T cell IL-2 receptor Cells Cultured Electrophoresis Agar Gel ZAP70 Cell Cycle DNA T lymphocyte Flow Cytometry Natural killer T cell Molecular biology medicine.anatomical_structure Endocrinology hormones hormone substitutes and hormone antagonists |
Zdroj: | European Journal of Immunology. 24:1061-1065 |
ISSN: | 1521-4141 0014-2980 |
DOI: | 10.1002/eji.1830240508 |
Popis: | 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. |
Databáze: | OpenAIRE |
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