Department of Neurology, Graduate School of Medicine, Chiba University, 1-8-1, Inohana, Chuo-ku, Chiba 260-8670, Japan.
Laboratory of Pharmacology and Toxicology, Graduate School of Pharmaceutical Sciences, Chiba University, 1-8-1, Inohana, Chuo-ku, Chiba 260-8670, Japan.
J Neuroimmunol. 2018 Mar 15;316:117-120. doi: 10.1016/j.jneuroim.2018.01.001. Epub 2018 Jan 3.
Serum soluble CD40 ligand (sCD40L) has been reported to positively correlate with the albumin quotient, a marker of blood-brain barrier (BBB) breakdown, in patients with multiple sclerosis (MS). To clarify the mechanisms of sCD40L in MS pathophysiology, sCD40L was administered to experimental autoimmune encephalomyelitis (EAE) mice and a human brain microvascular endothelial cell (HBMEC)-based BBB model. The high-dose sCD40L group showed a worse EAE score than the low-dose and control groups. BBB permeability was increased by administering sCD40L in a HBMEC-based BBB model. Thus, sCD40L induces more severe inflammation in the central nervous system by disrupting the BBB.
血清可溶性 CD40 配体 (sCD40L) 与血脑屏障 (BBB) 破坏的标志物白蛋白商呈正相关，已在多发性硬化症 (MS) 患者中报道。为了阐明 sCD40L 在 MS 病理生理学中的机制，将 sCD40L 给予实验性自身免疫性脑脊髓炎 (EAE) 小鼠和基于人脑血管内皮细胞 (HBMEC) 的 BBB 模型。高剂量 sCD40L 组的 EAE 评分比低剂量组和对照组差。在基于 HBMEC 的 BBB 模型中给予 sCD40L 可增加 BBB 通透性。因此，sCD40L 通过破坏 BBB 导致中枢神经系统更严重的炎症。
