Abstract
In the present study, we report that activated human astroglioma cells can injure T-lymphocytes by producing tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL). Treatment with lipopolysaccharides (LPS), a well-known immune stimulator, increased the expression levels of TRAIL mRNA and protein in human astroglioma cells. The increase of TRAIL mRNA expression by LPS was preceded by phosphorylation of the c-Jun N-terminal kinase (JNK) and consequently abrogated in the presence of the specific JNK inhibitor SP600125. The up-regulation of TRAIL expression was well co-related with AP-1 activation. Activated human astroglioma cells markedly induced the apoptotic death of T-lymphocytes. Pre-treatment with the TRAIL antagonistic protein TRAIL-R2:Fc prevented the death of T-lymphocytes caused by activated human astroglioma cells. The present results suggest that astroglioma cells may down-regulate T-lymphocytes via up-regulation of TRAIL.
| Original language | English |
|---|---|
| Pages (from-to) | 338-343 |
| Number of pages | 6 |
| Journal | Neuroscience Research |
| Volume | 54 |
| Issue number | 4 |
| DOIs | |
| Publication status | Published - 2006 Apr 1 |
| Externally published | Yes |
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Keywords
- Astroglioma
- c-Jun N-terminal kinase
- Cell death
- T-lymphocytes
- TRAIL
ASJC Scopus subject areas
- Neuroscience(all)
Cite this
Lipopolysaccharides-activated human astroglioma cells induce apoptotic death of T-lymphocytes via c-Jun N-terminal kinases-dependent up-regulation of TRAIL. / Kwon, Daeho; Cheong, Jae Hoon; Lee, Jae Chul; Kwon, Jae Hyun; Kim, Won-Ki.
In: Neuroscience Research, Vol. 54, No. 4, 01.04.2006, p. 338-343.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Lipopolysaccharides-activated human astroglioma cells induce apoptotic death of T-lymphocytes via c-Jun N-terminal kinases-dependent up-regulation of TRAIL
AU - Kwon, Daeho
AU - Cheong, Jae Hoon
AU - Lee, Jae Chul
AU - Kwon, Jae Hyun
AU - Kim, Won-Ki
PY - 2006/4/1
Y1 - 2006/4/1
N2 - In the present study, we report that activated human astroglioma cells can injure T-lymphocytes by producing tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL). Treatment with lipopolysaccharides (LPS), a well-known immune stimulator, increased the expression levels of TRAIL mRNA and protein in human astroglioma cells. The increase of TRAIL mRNA expression by LPS was preceded by phosphorylation of the c-Jun N-terminal kinase (JNK) and consequently abrogated in the presence of the specific JNK inhibitor SP600125. The up-regulation of TRAIL expression was well co-related with AP-1 activation. Activated human astroglioma cells markedly induced the apoptotic death of T-lymphocytes. Pre-treatment with the TRAIL antagonistic protein TRAIL-R2:Fc prevented the death of T-lymphocytes caused by activated human astroglioma cells. The present results suggest that astroglioma cells may down-regulate T-lymphocytes via up-regulation of TRAIL.
AB - In the present study, we report that activated human astroglioma cells can injure T-lymphocytes by producing tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL). Treatment with lipopolysaccharides (LPS), a well-known immune stimulator, increased the expression levels of TRAIL mRNA and protein in human astroglioma cells. The increase of TRAIL mRNA expression by LPS was preceded by phosphorylation of the c-Jun N-terminal kinase (JNK) and consequently abrogated in the presence of the specific JNK inhibitor SP600125. The up-regulation of TRAIL expression was well co-related with AP-1 activation. Activated human astroglioma cells markedly induced the apoptotic death of T-lymphocytes. Pre-treatment with the TRAIL antagonistic protein TRAIL-R2:Fc prevented the death of T-lymphocytes caused by activated human astroglioma cells. The present results suggest that astroglioma cells may down-regulate T-lymphocytes via up-regulation of TRAIL.
KW - Astroglioma
KW - c-Jun N-terminal kinase
KW - Cell death
KW - T-lymphocytes
KW - TRAIL
UR - http://www.scopus.com/inward/record.url?scp=33644852678&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=33644852678&partnerID=8YFLogxK
U2 - 10.1016/j.neures.2005.12.011
DO - 10.1016/j.neures.2005.12.011
M3 - Article
C2 - 16442178
AN - SCOPUS:33644852678
VL - 54
SP - 338
EP - 343
JO - Neuroscience Research
JF - Neuroscience Research
SN - 0168-0102
IS - 4
ER -