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

HLA and immunological features of SARS-CoV-2-induced Guillain-Barré syndrome.
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DOI:
10.1007/s10072-020-04787-7
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发表时间:
2020-12
期刊:
Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology
影响因子:
--
通讯作者:
Valente M
Valente M
中科院分区:
其他
文献类型:
--
作者:
Gigli GL;Vogrig A;Nilo A;Fabris M;Biasotto A;Curcio F;Miotti V;Tascini C;Valente M

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我们报告了一例SARS-CoV-2诱导的格林-巴利综合征(Si-GBS)的临床和免疫学特征,表明(1)即使在少症状COVID-19感染后也可发生Si-GBS;(2)独特的细胞因子谱与这种自身免疫性并发症相关,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)特定的遗传倾向可能是相关的,因为患者携带已知与GBS相关的几个HLA等位基因,包括独特的I类(HLA-A33)和II类等位基因(DRB 1 *03:01和DQB 1 *05:01)。据我们所知,这是第一例在CSF中检测到SARS-CoV-2抗体的GBS病例,进一步加强了病毒作为触发因素的作用。总之,我们的研究表明,即使在没有临床严重COVID-19感染的情况下,也需要在流行地区GBS患者的血清和CSF中寻找SARS-CoV-2抗体,并且IL-8途径可能与Si-GBS发病机制相关。需要进一步的研究来总结遗传发现的相关性,但HLA在这种情况下可能与其他自身免疫性神经综合征(包括感染引发的综合征)一样发挥作用。
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 (DRB1*03:01 and DQB1*05:01). 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.
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