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首页> 外文期刊>Journal of Neuroimmunology: Official Bulletin of the Research Committee on Neuroimmunology of the World Federation of Neurology >Inhibition of the adhesion step of leukodiapedesis: a critical event in the recovery of Guillain-Barre syndrome associated with accumulation of proteolytically active lymphocytes in blood.
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Inhibition of the adhesion step of leukodiapedesis: a critical event in the recovery of Guillain-Barre syndrome associated with accumulation of proteolytically active lymphocytes in blood.

机译：抑制白癜风的粘附步骤：与血液中蛋白水解活性淋巴细胞的积累有关的吉兰-巴雷综合征恢复的关键事件。

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摘要

Intraneural inflammation, that reflects emigration of immune cells from blood to nerve tissue, is a critical event in Guillain-Barre syndrome pathogenesis. To investigate the adhesion and transmigration phases of leukodiapedesis, we determined in a series of patients with GBS: (1) circulating levels of soluble forms of adhesion molecules (sICAM-1 and sVCAM-1); (2) attachment capacities of circulating lymphocytes to rICAM-1 and rVCAM-1; (3) fibronectin-penetrating capacities of circulating lymphocytes; and (4) lymphocyte intracellular concentrations of MMP-9 at the different phases of GBS and in healthy controls. Circulating levels of sVCAM-1 and sICAM-1 were above normal values at the time of progression, markedly increased at the time of plateau (sVCAM-1: P<0.03; sICAM-1: P<0.02), and tended to normalize during recovery. The percentage of cells with attachment capacities to rVCAM-1 and to rICAM-1 decreased from progression to recovery by 30 and 31%, respectively (P<0.02). The number of circulating lymphocytes with fibronectin penetrating capacities was lower than controls at the time of progression (P<0.01), then progressively increased to reach values higher than controls at the time of late recovery (P<0.02). Cellular concentrations of MMP-9 in circulating lymphocytes paralleled their fibronectin penetrating capacities. These results suggest early emigration of lymphocytes into nerve, followed by shedding of adhesion molecules from endothelium, and late decrease of lymphocyte adhesion capacities. Plateau and recovery are associated with accumulation in the vascular compartment of still proteolytically active lymphocytes that can no longer adhere to endothelial cells. Modulation of the adhesion step of leukodiapedesis may be crucially involved in the switch from progression to plateau of GBS.
机译：神经内炎症反映了免疫细胞从血液向神经组织的迁移，是格林-巴利综合征发病机理中的关键事件。为了研究白带硬化的粘附和转运阶段，我们在一系列患有GBS的患者中进行了确定：（1）循环水平的可溶性分子形式的粘附分子（sICAM-1和sVCAM-1）; （2）循环淋巴细胞对rICAM-1和rVCAM-1的附着能力; （3）循环淋巴细胞的纤连蛋白穿透能力; （4）GBS不同阶段和健康对照组的淋巴细胞MMP-9浓度。 sVCAM-1和sICAM-1的循环水平在进展时高于正常值，在高原时显着增加（sVCAM-1：P <0.03; sICAM-1：P <0.02），并在此期间趋于正常复苏。具有与rVCAM-1和rICAM-1结合能力的细胞百分比从进展到恢复分别降低了30％和31％（P <0.02）。具有纤连蛋白穿透能力的循环淋巴细胞数目在进展时低于对照组（P <0.01），然后逐渐增加，达到比在晚期恢复时更高的值（P <0.02）。循环淋巴细胞中MMP-9的细胞浓度与其纤连蛋白穿透能力平行。这些结果表明淋巴细胞早期迁移到神经中，然后从内皮脱落粘附分子，并且晚期淋巴细胞粘附能力降低。高原和恢复与仍然具有蛋白水解活性的淋巴细胞在血管腔室中的积累有关，这些淋巴细胞不再粘附于内皮细胞。从GBS的进展到平稳的转变中，白带硬化的粘附步骤的调节可能至关重要。

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