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SARS-CoV-2 诱导的吉兰-巴雷综合征的 HLA 和免疫学特征。

HLA and immunological features of SARS-CoV-2-induced Guillain-Barré syndrome.

机构信息

Clinical Neurology Unit, Santa Maria della Misericordia University Hospital, Piazzale Santa Maria della Misericordia, 15, 33010, Udine, Italy.

Department of Medicine (DAME), University of Udine Medical School, Udine, Italy.

出版信息

Neurol Sci. 2020 Dec;41(12):3391-3394. doi: 10.1007/s10072-020-04787-7.

Abstract

We report the clinical and immunological features in a case of SARS-CoV-2-induced Guillain-Barré syndrome (Si-GBS), suggesting that (1) Si-GBS can develop even after paucisymptomatic COVID-19 infection; (2) a distinctive cytokine repertoire is associated with this autoimmune complication, with increased CSF concentration of IL-8, and moderately increased serum levels of IL-6, IL-8, and TNF-α; (3) a particular genetic predisposition can be relevant, since the patient carried several HLA alleles known to be associated with GBS, including distinctive class I (HLA-A33) and class II alleles (DRB103:01 and DQB105:01). To the best of our knowledge, this is the first case of GBS in which SARS-CoV-2 antibodies were detected in the CSF, further strengthening the role of the virus as a trigger. In conclusion, our study suggests that SARS-CoV-2 antibodies need to be searched in the serum and CSF in patients with GBS living in endemic areas, even in the absence of a clinically severe COVID-19 infection, and that IL-8 pathway can be relevant in Si-GBS pathogenesis. Further studies are needed to conclude on the relevance of the genetic findings, but it is likely that HLA plays a role in this setting as in other autoimmune neurological syndromes, including those triggered by infections.

摘要

我们报告了一例由 SARS-CoV-2 引起的格林-巴利综合征(Si-GBS)的临床和免疫学特征,表明:(1)即使在 COVID-19 感染症状较轻的情况下,也可能发生 Si-GBS;(2)这种自身免疫性并发症与独特的细胞因子谱相关,CSF 中 IL-8 浓度升高,血清中 IL-6、IL-8 和 TNF-α 水平中度升高;(3)特定的遗传易感性可能与之相关,因为该患者携带了几个已知与 GBS 相关的 HLA 等位基因,包括独特的 I 类(HLA-A33)和 II 类等位基因(DRB103:01 和 DQB105:01)。据我们所知,这是首例在脑脊液中检测到 SARS-CoV-2 抗体的 GBS 病例,进一步证实了该病毒作为触发因素的作用。总之,我们的研究表明,在 GBS 患者中,即使没有临床上严重的 COVID-19 感染,也需要在血清和脑脊液中搜索 SARS-CoV-2 抗体,并且 IL-8 途径可能与 Si-GBS 的发病机制相关。需要进一步的研究来确定遗传发现的相关性,但 HLA 在这种情况下可能与其他自身免疫性神经综合征(包括由感染引起的综合征)一样发挥作用。

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