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白细胞介素 6:与 SARS-CoV-2 免疫病理学的相关性。

IL-6: Relevance for immunopathology of SARS-CoV-2.

机构信息

Laboratory of Molecular Mechanisms of Immunity, Engelhardt Institute of Molecular Biology, Russian Academy of Sciences, Moscow, Russia; Faculty of Biology, Lomonosov Moscow State University, Moscow, Russia.

Laboratory of Molecular Mechanisms of Immunity, Engelhardt Institute of Molecular Biology, Russian Academy of Sciences, Moscow, Russia; Faculty of Biology, Lomonosov Moscow State University, Moscow, Russia; Center for Precision Genome Editing and Genetic Technologies for Biomedicine, Engelhardt Institute of Molecular Biology, Russian Academy of Sciences, Moscow, Russia.

出版信息

Cytokine Growth Factor Rev. 2020 Jun;53:13-24. doi: 10.1016/j.cytogfr.2020.05.009. Epub 2020 May 20.

DOI:10.1016/j.cytogfr.2020.05.009
PMID:32475759
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7237916/
Abstract

COVID-19 mortality is strongly associated with the development of severe pneumonia and acute respiratory distress syndrome with the worst outcome resulting in cytokine release syndrome and multiorgan failure. It is becoming critically important to identify at the early stage of the infection those patients who are prone to develop the most adverse effects. Elevated systemic interleukin-6 levels in patients with COVID-19 are considered as a relevant parameter in predicting most severe course of disease and the need for intensive care. This review discusses the mechanisms by which IL-6 may possibly contribute to disease exacerbation and the potential of therapeutic approaches based on anti-IL-6 biologics.

摘要

COVID-19 死亡率与严重肺炎和急性呼吸窘迫综合征的发展密切相关,最严重的后果是细胞因子释放综合征和多器官衰竭。在感染的早期阶段识别那些容易出现最不利影响的患者变得至关重要。COVID-19 患者的系统性白细胞介素 6 水平升高被认为是预测最严重疾病过程和需要重症监护的相关参数。本文综述了白细胞介素 6 可能导致疾病恶化的机制,以及基于抗白细胞介素 6 生物制剂的治疗方法的潜力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3305/7237916/55efc77bf0d1/gr4_lrg.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3305/7237916/bff22f757716/gr1_lrg.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3305/7237916/addf245da896/gr2_lrg.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3305/7237916/90085cdcd6a4/gr3_lrg.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3305/7237916/55efc77bf0d1/gr4_lrg.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3305/7237916/bff22f757716/gr1_lrg.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3305/7237916/addf245da896/gr2_lrg.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3305/7237916/90085cdcd6a4/gr3_lrg.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3305/7237916/55efc77bf0d1/gr4_lrg.jpg

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Type 2 and interferon inflammation regulate SARS-CoV-2 entry factor expression in the airway epithelium.
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