Tumor necrosis factor-α and interleukin-6 regulate secretion of brain-derived neurotrophic factor in human monocytes
Tumor necrosis factor-α and interleukin-6 regulate secretion of brain-derived neurotrophic factor in human monocytes
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DOI：
10.1016/j.jneuroim.2004.10.026
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发表时间：
2005-03-01
影响因子：
3.3
通讯作者：
Braun, A
中科院分区：
文献类型：
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作者：
Schulte-Herbrüggen, O;Nassenstein, C;Braun, A
活化的巨噬细胞已被证明在多发性硬化症（MS）或过敏性支气管哮喘（BA）等疾病中产生脑源性神经营养因子（BDNF）。然而，关于BDNF在这些细胞中的调节的数据很少。我们证明未受刺激的人外周血单核细胞，而不是淋巴细胞，组成性地分泌BDNF。IL-6和tnf - α特异性地增强了单核细胞BDNF的分泌，而典型的Th1 -和th2细胞因子没有表现出任何影响。没有一种细胞因子能诱导T细胞或b细胞分泌BDNF。因此，我们的数据提供了证据，证明IL-6和tnf - α代表了炎症性疾病中单核细胞浸润和神经元变化之间的特定联系。(c) 2004 Elsevier B.V.版权所有
Activated macrophages have been shown to produce brain-derived neurotrophic factor (BDNF) in diseases such as multiple sclerosis (MS) or allergic bronchial asthma (BA). However, there is little data on BDNF regulation in these cells. We demonstrate that unstimulated human peripheral blood monocytes, but not lymphocytes, constitutively secrete BDNF. IL-6 and TNF-alpha specifically enhanced BDNF secretion in monocytes, whereas typical Th1 - and Th2-cytokines did not show any effect. None of the cytokines induced BDNF secretion in T- or B-cells. Thus, Our data provide evidence that IL-6 and TNF-alpha represent a specific link between monocyte infiltration and neuronal changes in inflammatory diseases. (c) 2004 Elsevier B.V. All rights reserved.