The possible role of peripherally generated cross-reactive IgG in breakdown of the blood–brain barrier and initiation of multiple sclerosis

Aram Mokarizadeh , Mohammad Abdollahi , Mohammad-Amin Rezvanfar , Mohammad-Reza Rahmani
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引用次数: 4

Abstract

The initiating event in multiple sclerosis (MS) pathogenesis is not known yet. However, in general, breakdown of the blood-brain barrier (BBB) and subsequent infiltration of immune cells into the central nervous system (CNS) has been thought to be the main initiating event. Nonetheless, the mechanism by which the BBB gets disrupted and allows immune cells to infiltrate into the CNS is not fully understood. Evidence indicates that prior to cellular infiltration, over passing peripherally generated cross-reactive immunoglobulin G (IgG) through the transiently permeable BBB during systemic inflammation, hypoxia, hyperthermia, transient hypertension or acute stresses may cause CNS inflammation, BBB breakdown and then initiation of MS disease. Here, we discuss the possible detailed mechanisms that may be involved in cross-reactive IgG-mediated MS autoimmunity.

Abstract Image

外周产生的交叉反应性IgG在血脑屏障破坏和多发性硬化症发生中的可能作用
多发性硬化(MS)发病机制的起始事件尚不清楚。然而,一般来说,血脑屏障(BBB)的破坏和随后免疫细胞渗入中枢神经系统(CNS)被认为是主要的起始事件。尽管如此,血脑屏障被破坏并允许免疫细胞渗入中枢神经系统的机制尚不完全清楚。有证据表明,在细胞浸润之前,在全身性炎症、缺氧、高热、短暂性高血压或急性应激时,外周产生的交叉反应性免疫球蛋白G (IgG)通过可瞬时渗透的血脑屏障,可引起中枢神经系统炎症、血脑屏障破坏,进而引发多发性硬化症。在这里,我们讨论了可能参与交叉反应性igg介导的MS自身免疫的详细机制。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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