a tnf receptor 2 selective agonist rescues human neurons from oxidative stress-induced cell death肿瘤坏死因子受体2选择性受体激动剂拯救人类神经元氧化应激细胞死亡.pdfVIP
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a tnf receptor 2 selective agonist rescues human neurons from oxidative stress-induced cell death肿瘤坏死因子受体2选择性受体激动剂拯救人类神经元氧化应激细胞死亡
A TNF Receptor 2 Selective Agonist Rescues Human
Neurons from Oxidative Stress-Induced Cell Death
1 1 1 2 1 1
Roman Fischer *, Olaf Maier , Martin Siegemund , Harald Wajant , Peter Scheurich , Klaus Pfizenmaier
1 Institute of Cell Biology and Immunology, University Stuttgart, Stuttgart, Germany, 2 Division of Molecular Internal Medicine, Department of Internal Medicine II,
¨ ¨
University Hospital Wurzburg, Wurzburg, Germany
Abstract
Tumor necrosis factor (TNF) plays a dual role in neurodegenerative diseases. Whereas TNF receptor (TNFR) 1 is
predominantly associated with neurodegeneration, TNFR2 is involved in tissue regeneration and neuroprotection.
Accordingly, the availability of TNFR2-selective agonists could allow the development of new therapeutic treatments of
neurodegenerative diseases. We constructed a soluble, human TNFR2 agonist (TNC-scTNFR2) by genetic fusion of the
trimerization domain of tenascin C to a TNFR2-selective single-chain TNF molecule, which is comprised of three TNF
domains connected by short peptide linkers. TNC-scTNFR2 specifically activated TNFR2 and possessed membrane-TNF
mimetic activity, resulting in TNFR2 signaling complex formation and activation of downstream signaling pathways.
Protection from neurodegeneration was assessed using the human dopaminergic neuronal cell line LUHMES. First we show
that TNC-scTNF interfered with cell death pathways subsequent to H O exposure. Protection from cell death was
R2
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