论文部分内容阅读
吉兰-巴雷综合征(GBS)的发病机理可能与存在 髓鞘素蛋白的循环抗体、外周血和周围神经的T淋巴细胞及局部和游走来的巨噬细胞的激活有关。局灶的和全身释放的细胞因子也可能发挥重要作用。转移生长因子(TGF-β1)是一种强有力的抗炎症性细胞因子,在中枢神经系统脱髓鞘疾病中,如多发性硬化复发时TGF-β1的产生减少。本文观察了GBS患者在恢复期前,即瘫痪进展及其后的病情稳定阶段血液中的促炎症性和抗炎症性细胞因子水平的变化。
The pathogenesis of Guillain-Barre syndrome (GBS) may be related to the presence of circulating antibodies to myelin, peripheral blood and peripheral nerve T lymphocytes, and local and migratory macrophages. Focal and systemic release of cytokines may also play an important role. Transforming growth factor (TGF-β1) is a potent anti-inflammatory cytokine that has been shown to reduce the production of TGF-β1 in central nervous system demyelinating diseases such as multiple sclerosis. This article examines the changes in blood levels of pro-inflammatory and anti-inflammatory cytokines in patients with GBS before recovery, ie, progression of paralysis and subsequent stabilization of disease.