Plumb Jonnie, Cross Alison K, Surr Jessica, Haddock Gail, Smith Terence, Bunning Rowena A D, Woodroofe M Nicola
Biomedical Research Centre, Sheffield Hallam University, Howard St., Sheffield, S1 1WB, United Kingdom.
J Neuroimmunol. 2005 Jul;164(1-2):1-9. doi: 10.1016/j.jneuroim.2005.02.021.
Tumour necrosis factor (TNF) is a major immunomodulatory and proinflammatory cytokine implicated in the pathogenesis of multiple sclerosis (MS) and the animal model experimental autoimmune encephalomyelitis (EAE). ADAM-17 cleaves membrane-bound TNF into its soluble form. The distribution and level of ADAM-17 expression within spinal cords of Lewis rats with EAE was investigated. ADAM-17 was associated with endothelial cells in the naïve and pre-disease spinal cords. In peak disease astrocytic and inflammatory cells expressed ADAM-17. Upregulation of ADAM-17 mRNA expression was coupled with a decrease in mRNA levels of its inhibitor TIMP3 suggesting a role for ADAM-17 in EAE pathogenesis.
肿瘤坏死因子（TNF）是一种主要的免疫调节和促炎细胞因子，与多发性硬化症（MS）及动物模型实验性自身免疫性脑脊髓炎（EAE）的发病机制有关。ADAM-17可将膜结合型TNF裂解为可溶性形式。本研究调查了EAE Lewis大鼠脊髓内ADAM-17的表达分布及水平。在未发病和疾病前期的脊髓中，ADAM-17与内皮细胞相关。在疾病高峰期，星形胶质细胞和炎性细胞表达ADAM-17。ADAM-17 mRNA表达上调，同时其抑制剂TIMP3的mRNA水平下降，提示ADAM-17在EAE发病机制中发挥作用。
