VASCULAR CELL-ADHESION MOLECULE-1 MODULATION BY TUMOR-NECROSIS-FACTOR IN EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS
VASCULAR CELL-ADHESION MOLECULE-1 MODULATION BY TUMOR-NECROSIS-FACTOR IN EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS
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DOI：
10.1016/0165-5728(94)90074-4
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发表时间：
1994-05-01
影响因子：
3.3
通讯作者：
RUDDLE, NH
中科院分区：
文献类型：
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作者：
BARTEN, DM;RUDDLE, NH
抗肿瘤坏死因子（TNF）抗体抑制SJL小鼠被动转移实验性变应性脑脊髓炎（EAE）。研究了这种情况通过干扰TNF上调内皮细胞粘附分子发生的可能性。脊髓血管上血管细胞黏附分子-1 （VCAM-1）和细胞间黏附分子-1 （ICAM-1）表达增加。抗tnf治疗可显著降低或阻止VCAM-1的上调。抗tnf治疗的白细胞浸润比患病动物低15倍。脊髓内皮细胞中VCAM-1的表达与T细胞、B细胞或单核细胞浸润程度呈正相关，而非ICAM-1或纤维连接蛋白。
Anti-tumor necrosis factor (TNF) antibodies inhibit passively transferred experimental allergic encephalomyelitis (EAE) in SJL mice. The possibility that this occurs through interference in TNF's upregulation of endothelial cell adhesion molecules was investigated. Expression of both vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1) on spinal cord vessels increased during EAE. The upregulation of VCAM-1 was markedly reduced or prevented by anti-TNF treatment. Leukocytic infiltration was 15-fold lower in anti-TNF-treated than diseased animals. Spinal cord endothelial expression of VCAM-1, though not ICAM-1 or fibronectin, positively correlated with the extent of T cell, B cell or monocyte infiltration in each animal.