CONDUCTION FAILURE AND NERVE-CONDUCTION SLOWING IN EXPERIMENTAL ALLERGIC NEURITIS INDUCED BY P2-SPECIFIC T-CELL LINES
CONDUCTION FAILURE AND NERVE-CONDUCTION SLOWING IN EXPERIMENTAL ALLERGIC NEURITIS INDUCED BY P2-SPECIFIC T-CELL LINES
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DOI：
10.1002/ana.410190109
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发表时间：
1986-01-01
影响因子：
11.2
通讯作者：
WEKERLE, H
中科院分区：
文献类型：
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作者：
HEININGER, K;STOLL, G;WEKERLE, H
P2特异性T细胞（LiP 2/A）介导刘易斯大鼠过继转移给幼稚受体后的实验性变态反应性神经炎（EAN）。在4天的潜伏期后，注射2 × 10 - 4 μ g/ml的生理盐水。106系细胞诱导周围神经和神经根的暴发性截瘫和完全传导失败，类似于急性轴突破坏。注射106个细胞引起较轻的临床体征、神经传导失败和传导减慢。临床和电生理恢复从过继转移EAN几乎是完全的，其时间进程呈负相关的EAN的初始严重程度。这些发现表明，由P2特异性T细胞系诱导的EAN可以以剂量依赖性方式导致深刻且快速发展的神经功能障碍。
P2-specific T cells (LiP2/A) mediate experimental allergic neuritis (EAN) in the Lewis rat after adoptive transfer to naive recipients. After a latent period of 4 days, injection of 2 .times. 106 line cells induced fulminant paraplegia and complete conduction failure in the peripheral nerves and roots, resembling acute axonal breakdown. Injection with 106 cells caused milder clinical signs, nerve conduction failure, and conduction slowing. Clinical and electrophysiological recovery from adoptively transferred EAN was nearly complete and its time course was inversely correlated to the initial severity of EAN. These findings suggest that EAN induced by the P2-specific T-cell line can lead to a profound and rapidly evolving nerve dysfunction in a dose-dependent fashion.