Archelos J J, Fortwängler T, Hartung H P
Department of Neurology, Julius-Maximilians-Universität Würzburg, Germany.
Neurosci Lett. 1997 Oct 10;235(1-2):9-12. doi: 10.1016/s0304-3940(97)00692-7.
The leukocyte adhesion molecule L-selectin plays a key role in the initial steps of transendothelial migration of T cells and monocytes. In this study we investigated the role of L-selectin in the pathogenesis of experimental autoimmune neuritis (EAN) an animal model of the Guillain-Barré syndrome. EAN was induced in Lewis rats by sensitization with peripheral nerve myelin. Treatment with HRL3, a monoclonal antibody to L-selectin, efficiently suppressed clinical signs of EAN. Histological examination of the peripheral nervous system (PNS) revealed a marked reduction of inflammatory infiltrates and demyelination during treatment with HRL3. We conclude that L-selectin-dependent mechanisms are of pathophysiological relevance in EAN. Modulation of L-selectin in vivo could be a novel therapeutic approach to autoimmune diseases of the PNS.
白细胞粘附分子L-选择素在T细胞和单核细胞跨内皮迁移的起始步骤中起关键作用。在本研究中，我们调查了L-选择素在实验性自身免疫性神经炎（EAN）发病机制中的作用，EAN是格林-巴利综合征的一种动物模型。通过用周围神经髓鞘致敏在Lewis大鼠中诱导EAN。用抗L-选择素单克隆抗体HRL3治疗可有效抑制EAN的临床症状。周围神经系统（PNS）的组织学检查显示，在用HRL3治疗期间，炎性浸润和脱髓鞘明显减少。我们得出结论，L-选择素依赖性机制在EAN中具有病理生理学相关性。体内调节L-选择素可能是治疗PNS自身免疫性疾病的一种新的治疗方法。
