研究揭示COVID-19患者腦脊液中T細胞衰竭和去分化單核細胞的神經學表現
作者：
小柯機器人發布時間：2020/12/25 14:42:42
近日，德國明斯特大學Gerd Meyer zu Hörste、Mark Stettner等研究人員合作揭示COVID-19患者腦脊液中T細胞衰竭和去分化單核細胞的神經學表現。2020年12月23日，《免疫》雜誌在線發表了這項成果。
研究人員表示，COVID-19患者會出現神經系統後遺症，例如頭痛、神經炎或腦血管疾病。這些情況（Neuro-COVID）在嚴重COVID-19患者中更為常見。
為了了解這些神經系統後遺症的病因，研究人員利用單細胞測序並檢查了與非炎性和自身免疫性神經系統疾病或病毒性腦炎患者相比，Neuro-COVID患者腦脊液（CSF）的免疫細胞譜。Neuro-COVID患者的CSF表現為去分化單核細胞和耗盡的CD4+T細胞擴增。Neuro-COVID CSF白細胞具有豐富的幹擾素特徵。但是，這沒有病毒性腦炎那麼明顯。細胞庫分析顯示，與輕度的Neuro-COVID患者相比，嚴重者的克隆性T細胞擴增廣泛、幹擾素反應減弱。
總的來說，這些發現記錄了Neuro-COVID患者的CSF免疫區室，並提示在這種情況下抗病毒反應受到損害。
附：英文原文
Title: Neurological Manifestations of COVID-19 Feature T Cell Exhaustion and Dedifferentiated Monocytes in Cerebrospinal Fluid
Author: Michael Heming, Xiaolin Li, Saskia Ruber, Anne K. Mausberg, Anna-Lena Brsch, Maike Hartlehnert, Arpita Singhal, I-Na Lu, Michael Fleischer, Fabian Szepanowski, Oliver Witzke, Thorsten Brenner, Ulf Dittmer, Nir Yosef, Christoph Kleinschnitz, Heinz Wiendl, Mark Stettner, Gerd Meyer zu Hrste
Issue&Volume: 2020-12-22
Abstract: Patients suffering from Coronavirus disease 2019 (COVID-19) can develop neurological sequelae, such as headache, neuroinflammatory or cerebrovascular disease. These conditions - here termed Neuro-COVID - are more frequent in patients with severe COVID-19. To understand the etiology of these neurological sequelae, we utilized single-cell sequencing and examined the immune cell profiles from the cerebrospinal fluid (CSF) of Neuro-COVID patients compared to patients with non-inflammatory and autoimmune neurological diseases or with viral encephalitis. The CSF of Neuro-COVID patients exhibited an expansion of dedifferentiated monocytes and of exhausted CD4+ T cells. Neuro-COVID CSF leukocytes featured an enriched interferon signature; however, this was less pronounced than in viral encephalitis. Repertoire analysis revealed broad clonal T cell expansion and curtailed interferon response in severe compared to mild Neuro-COVID patients. Collectively, our findings document the CSF immune compartment in Neuro-COVID patients and suggest compromised antiviral responses in this setting.
DOI: 10.1016/j.immuni.2020.12.011
Source: https://www.cell.com/immunity/fulltext/S1074-7613(20)30539-2