T cell receptor-independent apoptosis of thymocyte clones induced by a thymic epithelial cell line is mediated by steroids

Yael Zilberman*, Eitan Yefenof, Esther Oron, Anna Dorogin, Rina Guy

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

31 Scopus citations

Abstract

We have studied the mechanisms involved in TcR-independent apoptosis of radiation leukemia virus (RadLV)-transformed thymocyte clones induced by a thymic epithelial cell line (TEC). TEC induced apoptosis of an immature CD4+8+3+ (PD1.6) but not of a CD4+8+3+ (B10) thymocyte clone. TEC- derived conditioned medium did not mimic the signal induced by TEC in PD1.6 cells. However, the TEC-resistant clone B10 apoptosed in response to TEC, provided that PD1.6 cells were also present in the culture. This effect on bystander cells suggests that a secreted factor was involved. The involvement of glucocorticoid hormones as potential mediators was addressed. PD1.6 cells apoptosed in response to dexamethasone or a cell-permeating analog of cAMP, while B10 cells were relatively resistant to dexamethasone. TcR cross- linking inhibited both TEC- and dexamethasone- but not cAMP-induced apoptosis. Aminoglutethimide and Ru38486 inhibited TEC-induced apoptosis of PD1.6 cells, whereas Ru28318 had a negligible effect. The results suggest that steroid hormones are involved in TcR-independent apoptosis of immature double-positive thymocyte clones induced by TEC.

Original languageEnglish
Pages (from-to)78-84
Number of pages7
JournalCellular Immunology
Volume170
Issue number1
DOIs
StatePublished - 25 May 1996

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