脊髓灰质炎后患者血清免疫复合物水平正常

Eva Melin , Azita Sohrabian , Johan Rönnelid , Kristian Borg
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引用次数: 6

摘要

目的脊髓灰质炎后综合征的病理生理机制尚不完全清楚。脑脊液和外周血细胞因子水平升高提示系统性炎症过程。细胞因子水平下降和静脉注射免疫球蛋白治疗的临床效果进一步表明炎症/免疫发病机制。本研究的目的是通过分析免疫复合物来评估初始感染后是否存在自身免疫过程。方法对20例脊髓灰质炎后患者和95例健康对照者的血液循环免疫复合物进行分析。为了弥补患者和对照组之间的年龄差异,只使用30名年龄最大的对照组进行亚分析。比较脊髓灰质炎后患者与10名健康对照者聚乙二醇沉淀免疫复合物诱导肿瘤坏死因子的特性。结果脊髓灰质炎后患者与整个对照组(包括30名最年长的调查对象)的水平比较,差异无统计学意义。免疫复合物诱导的肿瘤坏死因子水平与对照组比较无差异。结论脊髓灰质炎后患者的循环免疫复合物和循环免疫复合物诱导肿瘤坏死因子的作用与健康对照无明显差异,提示脊髓灰质炎后综合征不是由自身免疫反应引起的。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Normal serum levels of immune complexes in postpolio patients

Normal serum levels of immune complexes in postpolio patients

Normal serum levels of immune complexes in postpolio patients

Objective

The pathophysiology of the postpolio syndrome is not fully understood. Increased cytokine levels in cerebrospinal fluid and peripheral blood indicate a systemic inflammatory process. Decreased cytokine levels and the clinical effect of intravenous immunoglobulin treatment further indicate an inflammatory/immunological pathogenesis. The aim of the present study was to evaluate whether an autoimmune process follows the initial infection, by means of analyzing immune complexes.

Patients and methods

Circulating immune complexes were analyzed from blood samples of 20 postpolio patients and 95 healthy controls. To compensate for differences in age between patients and controls, a sub-analysis was performed using only the 30 oldest controls. Tumor necrosis factor-inducing properties of polyethylene glycol-precipitated immune complexes were compared between the postpolio patients and 10 healthy controls.

Results

When comparing levels in postpolio patients to the whole control group, including the 30 oldest investigated, there were no statistically significant differences. No difference was found in tumor necrosis factor levels induced by immune complexes when comparing patients and controls.

Conclusions

There was no increase in circulating immune complex or in tumor necrosis factor-inducing effects of circulating immune complex between postpolio patients and healthy controls, indicating that the postpolio syndrome is not due to an autoimmune reaction.

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