Abstract：
:Cardiotoxin-III (CTX-III), a major cardiotoxin isolated from the venom of the Taiwan cobra (Naja naja atra), is a highly basic, hydrophobic, toxic protein, which can induce lysis of mononuclear cells by an unknown mechanism. This study was undertaken to investigate the effects of CTX-III on untreated and PHA-activated peripheral blood mononuclear cells (PBMCs) in vitro. The results show that treatment of PHA-activated lymphocytes with CTX-III (10 microg/ml) induced apoptosis and depletion of the CD8(+) population. In both untreated and PHA-treated lymphocytes, interferon-gamma production was dramatically reduced and interleukin-2 (IL-2) production was moderately reduced by CTX-III treatment. In PHA-activated lymphocytes, CD4 expression was increased, whereas CD8 and IL-2R beta chain (CD25) expression were decreased. In contrast, CTX-III had no effect on the viability of PHA-activated monocytes but significantly enhanced their tumor necrosis factor-alpha production. These results show that CTX-III selectively enhanced activation-induced apoptosis in CD8(+) T cells. CTX-III was found to bind to the cell membrane of PHA-stimulated PBMCs, and three CTX-III-binding proteins, with molecular weights of 92, 77, and 68 kDa, were identified. We therefore propose that CTX-III interacts with one or more cell surface proteins and initiates a signal pathway causing functional changes. These findings provide an insight into the immunomodulatory properties of CTX-III and suggest a novel method for the selective induction of apoptosis in CD8(+) T lymphocytes.
journal_name
Toxicol Appl Pharmacoljournal_title
Toxicology and applied pharmacologyauthors
Su SH,Su SJ,Lin SR,Chang KLdoi
10.1016/s0041-008x(03)00327-2subject
Has Abstractpub_date
2003-11-15 00:00:00pages
97-105issue
1eissn
0041-008Xissn
1096-0333pii
S0041008X03003272journal_volume
193pub_type
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journal_title：Toxicology and applied pharmacology
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journal_title：Toxicology and applied pharmacology
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journal_title：Toxicology and applied pharmacology
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journal_title：Toxicology and applied pharmacology
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journal_title：Toxicology and applied pharmacology
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journal_title：Toxicology and applied pharmacology
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abstract：:Isoflurane is known to increase β-amyloid aggregation and neuronal damage. We hypothesized that isoflurane will have similar effects on the polyglutamine huntingtin protein and will cause alterations in intracellular calcium homeostasis. We tested this hypothesis in striatal cells from the expanded glutamine huntingti...
journal_title：Toxicology and applied pharmacology
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更新日期：2011-02-01 00:00:00
