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Pathogenic T-cells and inflammatory monocytes incite inflammatory storms in severe COVID-19 patients.致病性T细胞和炎性单核细胞在重症COVID-19患者中引发炎症风暴。
Natl Sci Rev. 2020 Jun;7(6):998-1002. doi: 10.1093/nsr/nwaa041. Epub 2020 Mar 13.
2
Network-Based Analysis of Fatal Comorbidities of COVID-19 and Potential Therapeutics.基于网络的 COVID-19 致死合并症分析及潜在治疗方法。
IEEE/ACM Trans Comput Biol Bioinform. 2021 Jul-Aug;18(4):1271-1280. doi: 10.1109/TCBB.2021.3075299. Epub 2021 Aug 6.
3
A systematic review of antibody mediated immunity to coronaviruses: kinetics, correlates of protection, and association with severity.冠状病毒抗体介导免疫的系统评价:动力学、保护相关性及与严重程度的关系。
Nat Commun. 2020 Sep 17;11(1):4704. doi: 10.1038/s41467-020-18450-4.
4
A single-cell atlas of the peripheral immune response in patients with severe COVID-19.严重 COVID-19 患者外周免疫反应的单细胞图谱。
Nat Med. 2020 Jul;26(7):1070-1076. doi: 10.1038/s41591-020-0944-y. Epub 2020 Jun 8.
5
Interleukin-1 blockade with high-dose anakinra in patients with COVID-19, acute respiratory distress syndrome, and hyperinflammation: a retrospective cohort study.在患有新冠肺炎、急性呼吸窘迫综合征和炎症反应过度的患者中使用高剂量阿那白滞素进行白细胞介素-1阻断:一项回顾性队列研究。
Lancet Rheumatol. 2020 Jun;2(6):e325-e331. doi: 10.1016/S2665-9913(20)30127-2. Epub 2020 May 7.
6
Distribution of ACE2, CD147, CD26, and other SARS-CoV-2 associated molecules in tissues and immune cells in health and in asthma, COPD, obesity, hypertension, and COVID-19 risk factors.在健康人群以及哮喘、COPD、肥胖、高血压和 COVID-19 危险因素患者的组织和免疫细胞中,ACE2、CD147、CD26 和其他 SARS-CoV-2 相关分子的分布。
Allergy. 2020 Nov;75(11):2829-2845. doi: 10.1111/all.14429. Epub 2020 Aug 24.
7
SARS-CoV-2 infection and overactivation of Nlrp3 inflammasome as a trigger of cytokine "storm" and risk factor for damage of hematopoietic stem cells.严重急性呼吸综合征冠状病毒 2 感染和 Nlrp3 炎性小体过度激活作为细胞因子“风暴”的触发因素和造血干细胞损伤的危险因素。
Leukemia. 2020 Jul;34(7):1726-1729. doi: 10.1038/s41375-020-0887-9. Epub 2020 Jun 1.
8
Targets of T Cell Responses to SARS-CoV-2 Coronavirus in Humans with COVID-19 Disease and Unexposed Individuals.COVID-19 疾病患者和未接触者体内针对 SARS-CoV-2 冠状病毒的 T 细胞反应的靶标。
Cell. 2020 Jun 25;181(7):1489-1501.e15. doi: 10.1016/j.cell.2020.05.015. Epub 2020 May 20.
9
Reduction and Functional Exhaustion of T Cells in Patients With Coronavirus Disease 2019 (COVID-19).新型冠状病毒病(COVID-19)患者 T 细胞减少和功能耗竭。
Front Immunol. 2020 May 1;11:827. doi: 10.3389/fimmu.2020.00827. eCollection 2020.
10
Pulmonary fibrosis and COVID-19: the potential role for antifibrotic therapy.肺纤维化与 COVID-19:抗纤维化治疗的潜在作用。
Lancet Respir Med. 2020 Aug;8(8):807-815. doi: 10.1016/S2213-2600(20)30225-3. Epub 2020 May 15.

新型冠状病毒病的免疫学:机制、临床转归、诊断和展望——欧洲过敏与临床免疫学会(EAACI)的报告。

Immunology of COVID-19: Mechanisms, clinical outcome, diagnostics, and perspectives-A report of the European Academy of Allergy and Clinical Immunology (EAACI).

机构信息

Swiss Institute of Allergy and Asthma Research (SIAF), University of Zurich, Davos, Switzerland.

Christine Kühne - Center for Allergy Research and Education (CK-CARE), Davos, Switzerland.

出版信息

Allergy. 2020 Oct;75(10):2445-2476. doi: 10.1111/all.14462.

DOI:10.1111/all.14462
PMID:32584441
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7361752/
Abstract

With the worldwide spread of the novel severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) resulting in declaration of a pandemic by the World Health Organization (WHO) on March 11, 2020, the SARS-CoV-2-induced coronavirus disease-19 (COVID-19) has become one of the main challenges of our times. The high infection rate and the severe disease course led to major safety and social restriction measures worldwide. There is an urgent need of unbiased expert knowledge guiding the development of efficient treatment and prevention strategies. This report summarizes current immunological data on mechanisms associated with the SARS-CoV-2 infection and COVID-19 development and progression to the most severe forms. We characterize the differences between adequate innate and adaptive immune response in mild disease and the deep immune dysfunction in the severe multiorgan disease. The similarities of the human immune response to SARS-CoV-2 and the SARS-CoV and MERS-CoV are underlined. We also summarize known and potential SARS-CoV-2 receptors on epithelial barriers, immune cells, endothelium and clinically involved organs such as lung, gut, kidney, cardiovascular, and neuronal system. Finally, we discuss the known and potential mechanisms underlying the involvement of comorbidities, gender, and age in development of COVID-19. Consequently, we highlight the knowledge gaps and urgent research requirements to provide a quick roadmap for ongoing and needed COVID-19 studies.

摘要

随着新型严重急性呼吸综合征冠状病毒 2(SARS-CoV-2)在全球范围内的传播,世界卫生组织(WHO)于 2020 年 3 月 11 日宣布大流行,由 SARS-CoV-2 引起的冠状病毒病 19(COVID-19)已成为我们这个时代的主要挑战之一。高感染率和严重的疾病过程导致全球范围内采取了重大的安全和社会限制措施。迫切需要公正的专家知识来指导高效治疗和预防策略的制定。本报告总结了目前关于 SARS-CoV-2 感染和 COVID-19 发展及进展为最严重形式的相关免疫机制的免疫学数据。我们描述了轻度疾病中适当的先天和适应性免疫反应与严重多器官疾病中深度免疫功能障碍之间的差异。强调了人类对 SARS-CoV-2、SARS-CoV 和 MERS-CoV 的免疫反应的相似性。我们还总结了已知和潜在的 SARS-CoV-2 在上皮屏障、免疫细胞、内皮和临床相关器官(如肺、肠道、肾脏、心血管和神经元系统)上的受体。最后,我们讨论了发病过程中合并症、性别和年龄的已知和潜在机制。因此,我们强调了知识差距和紧迫的研究需求,为正在进行和需要的 COVID-19 研究提供了快速路线图。