Department of Neurology, Neurological Institute, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.
Mult Scler. 2010 Oct;16(10):1178-88. doi: 10.1177/1352458510375706. Epub 2010 Jul 23.
Within multiple sclerosis lesions, brain-derived neurotrophic factor is detected in neurons and immunocytes.
To clarify brain-derived neurotrophic factor production by peripheral blood immunocytes and its relationship with clinical parameters in multiple sclerosis.
Serum brain-derived neurotrophic factor levels were measured by conventional enzyme-linked immunosorbent assay while brain-derived neurotrophic factor production by immunocytes was determined by an in situ enzyme-linked immunosorbent assay in 74 multiple sclerosis patients, 32 healthy controls, and 86 patients with other neurological diseases. The tyrosine kinase receptor TrkB expression level in peripheral blood mononuclear cells was measured by real-time polymerase chain reaction.
Multiple sclerosis patients showed significantly higher serum brain-derived neurotrophic factor levels than healthy controls and patients with other neurological diseases. Multiple sclerosis patients with high brain-derived neurotrophic factor levels were younger, and showed fewer relapse numbers than those with low brain-derived neurotrophic factor levels. Brain-derived neurotrophic factor production by T cells increased with age in healthy controls, but not in multiple sclerosis patients. Interferon beta induced a significant increase in serum brain-derived neurotrophic factor levels. Brain-derived neurotrophic factor production from T cells and TrkB expression levels in peripheral blood mononuclear cells were significantly enhanced in interferon beta-treated multiple sclerosis patients compared with untreated ones.
A high brain-derived neurotrophic factor level is related to early mild disease in young multiple sclerosis patients. Interferon beta potentiates brain-derived neurotrophic factor production and brain-derived neurotrophic factor receptor expression in peripheral blood mononuclear cells, which may act beneficially.
在多发性硬化症病变中，脑源性神经营养因子可在神经元和免疫细胞中检测到。
阐明外周血免疫细胞中脑源性神经营养因子的产生及其与多发性硬化症临床参数的关系。
通过常规酶联免疫吸附试验测量血清脑源性神经营养因子水平，通过原位酶联免疫吸附试验测定免疫细胞中脑源性神经营养因子的产生，共纳入 74 例多发性硬化症患者、32 名健康对照者和 86 名其他神经疾病患者。通过实时聚合酶链反应测定外周血单个核细胞中酪氨酸激酶受体 TrkB 的表达水平。
多发性硬化症患者的血清脑源性神经营养因子水平明显高于健康对照者和其他神经疾病患者。脑源性神经营养因子水平高的多发性硬化症患者较脑源性神经营养因子水平低的患者更年轻，复发次数更少。健康对照者中 T 细胞的脑源性神经营养因子产生随年龄增加而增加，但多发性硬化症患者中则不然。干扰素β可显著增加血清脑源性神经营养因子水平。与未治疗者相比，经干扰素β治疗的多发性硬化症患者 T 细胞脑源性神经营养因子产生和外周血单个核细胞中 TrkB 表达水平显著增强。
高脑源性神经营养因子水平与年轻多发性硬化症患者的早期轻度疾病有关。干扰素β增强外周血单个核细胞中脑源性神经营养因子的产生和脑源性神经营养因子受体表达，可能具有有益作用。
