Role of cytokines and Toll-like receptors in the immunopathogenesis of Guillain-Barré syndrome.

Role of cytokines and Toll-like receptors in the immunopathogenesis of Guillain-Barré syndrome.
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DOI:
10.1155/2014/758639
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发表时间:
2014
影响因子:
4.6
通讯作者:
Prasad KN
Prasad KN
中科院分区:
医学3区
文献类型:
--
作者:
Nyati KK;Prasad KN

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格林-巴罗综合征(GBS)是一种周围神经系统的自身免疫性疾病,主要由对传染性病原体的异常免疫反应引起。虽然有几种感染与GBS的发病机制有关,但并非所有受感染的个体都会患上这种疾病。此外,单一病原体感染也可能导致GBS的不同亚型,强调宿主因素在GBS发展中的作用。宿主因子调节广泛的炎症过程,这些炎症过程参与了包括GBS在内的自身免疫性疾病的发病机制。有证据表明,全身和局部释放的细胞因子及其参与免疫介导的脱髓鞘和周围神经轴突损伤在GBS的发病机制中起重要作用。toll样受体(TLRs)通过几种促炎细胞因子的转录连接先天免疫和适应性免疫。TLR基因可能增加对微生物感染的易感性;由于基因突变,对抗原的免疫反应减弱,细胞因子下调。在此,我们讨论宿主因子如细胞因子和tlr的关键作用,激活免疫反应,并参与疾病的发病机制。
Guillain-Barré syndrome (GBS) is an autoimmune disease of the peripheral nervous system, mostly triggered by an aberrant immune response to an infectious pathogen. Although several infections have been implicated in the pathogenesis of GBS, not all such infected individuals develop this disease. Moreover, infection with a single agent might also lead to different subtypes of GBS emphasizing the role of host factors in the development of GBS. The host factors regulate a broad range of inflammatory processes that are involved in the pathogenesis of autoimmune diseases including GBS. Evidences suggest that systemically and locally released cytokines and their involvement in immune-mediated demyelination and axonal damage of peripheral nerves are important in the pathogenesis of GBS. Toll-like receptors (TLRs) link innate and adaptive immunity through transcription of several proinflammatory cytokines. TLR genes may increase susceptibility to microbial infections; an attenuated immune response towards antigen and downregulation of cytokines occurs due to mutation in the gene. Herein, we discuss the crucial role of host factors such as cytokines and TLRs that activate the immune response and are involved in the pathogenesis of the disease.
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