维生素B12（钴胺素）缺乏性中枢神经病大鼠脑脊液中CD40:CD40配体二元体水平升高。
Increased levels of the CD40:CD40 ligand dyad in the cerebrospinal fluid of rats with vitamin B12(cobalamin)-deficient central neuropathy.
作者信息
Veber Daniela, Mutti Elena, Galmozzi Enrico, Cedrola Sabrina, Galbiati Stefania, Morabito Alberto, Tredici Giovanni, La Porta Caterina A, Scalabrino Giuseppe
机构信息
Institute of General Pathology and Center of Excellence on Neurodegenerative Diseases, University of Milan, via Mangiagalli 31, 20133 Milano, Italy.
出版信息
J Neuroimmunol. 2006 Jul;176(1-2):24-33. doi: 10.1016/j.jneuroim.2006.04.002. Epub 2006 May 22.
The levels of the soluble (s) CD40:sCD40 ligand (L) dyad, which belongs to the tumor necrosis factor (TNF)-alpha:TNF-alpha-receptor superfamily, are significantly increased in the cerebrospinal fluid (CSF), but not the serum of cobalamin (Cbl)-deficient (Cbl-D) rats. They were normalized or significantly reduced after treatment with Cbl, transforming growth factor-beta1 or S-adenosyl-L-methionine, and the normal myelin ultrastructure of the spinal cord was concomitantly restored. The concomitance of the two beneficial effects of these treatments strongly suggests that the increases in CSF sCD40:sCD40L levels may participate in the pathogenesis of purely myelinolytic Cbl-D central neuropathy in the rat. In keeping with this, an anti-CD40 treatment prevented myelin lesions.
可溶性（s）CD40：sCD40配体（L）二元体属于肿瘤坏死因子（TNF）-α：TNF-α受体超家族，其水平在钴胺素（Cbl）缺乏（Cbl-D）大鼠的脑脊液（CSF）中显著升高，但在血清中未升高。用Cbl、转化生长因子-β1或S-腺苷-L-甲硫氨酸治疗后，它们恢复正常或显著降低，同时脊髓的正常髓鞘超微结构也得以恢复。这些治疗的两种有益效果同时出现，强烈表明CSF中sCD40：sCD40L水平的升高可能参与了大鼠单纯性脱髓鞘性Cbl-D中枢神经病变的发病机制。与此一致的是，抗CD40治疗可预防髓鞘损伤。
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