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Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death
Published on: December 27, 2016
Glucocorticoid-induced apoptosis in the thymus
1Department of Microbiology and Immunology, University of Colorado Medical School, Denver 80262.
Seminars in Immunology
|December 1, 1992
Summary
Adrenal glucocorticoids induce apoptosis in immature thymus cells (thymocytes). This cell death process requires new gene and protein synthesis, suggesting regulation by endogenous glucocorticoids.
Area of Science:
- Immunology
- Endocrinology
- Cell Biology
Background:
- Adrenal glucocorticoids are known to affect thymus cells.
- Immature lymphocytes, specifically CD4/CD8 double-positive thymocytes, are the primary targets.
Purpose of the Study:
- To detail the mechanism of glucocorticoid-induced thymocyte death.
- To investigate the molecular requirements for this process.
- To explore the role of endogenous glucocorticoids in regulating thymocyte apoptosis.
Main Methods:
- In vivo and in vitro studies of thymocyte cell death.
- Characterization of apoptotic morphological changes.
- Investigation of mRNA and protein synthesis requirements.
Main Results:
- Glucocorticoid-induced thymocyte death is a form of apoptosis.
- Apoptosis is characterized by cell shrinkage, membrane changes, nuclear collapse, and DNA fragmentation.
- New mRNA and protein synthesis are essential for this cell death pathway.
- Initial steps taken to identify involved genes.
Conclusions:
- Glucocorticoid-induced thymocyte death is a well-defined apoptotic process.
- The process is dependent on de novo gene and protein synthesis.
- Endogenous glucocorticoids likely regulate the death of unselected thymocytes in vivo.
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