Interferon beta-1a induces expression of brain-derived neurotrophic factor in human T lymphocytes in vitro and not in vivo

IF 0.6 Q4 CLINICAL NEUROLOGY
Zarlascht Karmand, H. Hartung, O. Neuhaus
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引用次数: 3

Abstract

Aim: To detect IFN β-1a-induced expression of brain-derived neurotrophic factor (BDNF) to undermine the hypothesis of IFN β-1a-associated neuroprotection in multiple sclerosis (MS). Methods: The influence of IFN β-1a on in vitro activated peripheral blood lymphocytes from healthy donors was tested. Proliferation analyses were made to detect T-cell growth. BDNF expression was measured by standard ELISA. To assess the influence of IFN β-1a on BDNF expression in vivo, BDNF serum levels of MS patients treated with IFN β-1a were compared with those of untreated patients. Results: IFN β-1a inhibited T-cell proliferation dose dependently. It induced BDNF expression at middle concentrations. MS patients treated with IFN β-1a exhibited significantly lower BDNF serum levels than untreated patients. Conclusion: IFN β-1a may promote neuroprotection by inducing BDNF expression, but its importance in vivo remains open.
干扰素β-1a在体外和非体内诱导人T淋巴细胞表达脑源性神经营养因子
目的:检测干扰素β1a诱导的脑源性神经营养因子(BDNF)的表达,以破坏干扰素β1a对多发性硬化症(MS)相关神经保护的假说。方法:检测干扰素β-1a对健康献血员体外活化的外周血淋巴细胞的影响。进行增殖分析以检测T细胞的生长。通过标准ELISA测定BDNF的表达。为了评估IFNβ-1a对体内BDNF表达的影响,将接受IFNβ-1 a治疗的MS患者和未接受治疗的患者的BDNF血清水平进行比较。结果:IFNβ-1a对T细胞增殖具有剂量依赖性抑制作用。它在中等浓度下诱导BDNF的表达。接受IFNβ-1a治疗的MS患者的BDNF血清水平明显低于未接受治疗的患者。结论:IFNβ-1a可能通过诱导BDNF表达来促进神经保护作用,但其在体内的重要性尚不明确。
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来源期刊
Future Neurology
Future Neurology CLINICAL NEUROLOGY-
CiteScore
2.10
自引率
0.00%
发文量
10
期刊介绍: The neurological landscape is changing rapidly. From the technological perspective, advanced molecular approaches and imaging modalities have greatly increased our understanding of neurological disease, with enhanced prospects for effective treatments in common but very serious disorders such as stroke, epilepsy, multiple sclerosis and Parkinson’s disease. Nevertheless, at the same time, the healthcare community is increasingly challenged by the rise in neurodegenerative diseases consequent upon demographic changes in developed countries.
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