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Expression of TRAIL receptors in human autoreactive and foreign antigen-specific T cells.
- Source :
-
Cell Death & Differentiation . Jul2000, Vol. 7 Issue 7, p637. 8p. - Publication Year :
- 2000
-
Abstract
- Deletion of T cells due to apoptosis induction is a regulatory mechanism in the human immune system that may be impaired in autoimmune diseases such as multiple sclerosis (MS). Involvement of the apoptosis-mediating CD95/CD95 ligand system in MS has been demonstrated. Here, we report that (auto)antigen-specific human T cells are not killed in vitro by soluble TNF-related apoptosis-inducing ligand (TRAIL) although expressing death-inducing receptors, TRAIL receptor 1 (TRAIL-R1) and TRAIL-R2. Apoptosis was assessed by caspase activation and DNA fragmentation, receptor expression was detected by RT-PCR and flow cytometry. The (auto)antigen-specific T cells were also resistant to specific TRAIL-R1/TRAIL-R2-directed induction of apoptosis, indicating that coexpression of the truncated TRAIL-R3 and TRAILR4 in these T cells is not responsible for the observed resistance. Upon stimulation, levels of death-inducing TRAIL receptors decreased whereas TRAIL was up-regulated on the cell surface. In contrast to CD95, the role of TRAIL receptors in MS might not involve regulation of T cell vulnerability. [ABSTRACT FROM AUTHOR]
- Subjects :
- *APOPTOSIS
*IMMUNE system
*AUTOIMMUNE diseases
*MULTIPLE sclerosis
Subjects
Details
- Language :
- English
- ISSN :
- 13509047
- Volume :
- 7
- Issue :
- 7
- Database :
- Academic Search Index
- Journal :
- Cell Death & Differentiation
- Publication Type :
- Academic Journal
- Accession number :
- 8851423
- Full Text :
- https://doi.org/10.1038/sj.cdd.4400692