Monocytes and Macrophages in COVID-19.
Monocytes and Macrophages in COVID-19.
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DOI：
10.3389/fimmu.2021.720109
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发表时间：
2021
影响因子：
7.3
通讯作者：
Schulte-Schrepping J
中科院分区：
文献类型：
--
作者：
Knoll R;Schultze JL;Schulte-Schrepping J
COVID-19是一种由SARS-CoV-2引起的传染性病毒性疾病，导致了一场持续的大流行，对全球健康和社会经济造成了巨大影响。该疾病的特征主要但不完全在于呼吸道临床表现，其范围从轻度普通感冒症状（包括咳嗽和发烧）到严重呼吸窘迫和多器官衰竭。巨噬细胞是一组异质性的卵黄囊来源的单核吞噬细胞，存在于所有哺乳动物器官中，具有复杂的个体发育，在发育，稳态和宿主防御过程中发挥关键作用，具有组织依赖的可塑性。在感染的情况下，它们负责早期病原体识别、炎症的引发和消退以及组织损伤的修复。单核细胞，骨髓来源的血液驻留吞噬细胞，在病理条件下，如病毒感染，被招募到受影响的组织，以保护生物体免受入侵的病原体，并帮助有效解决炎症。鉴于它们在宿主防御中的关键作用以及它们失调的过度炎症所带来的潜在危险，了解COVID-19中的单核细胞和巨噬细胞表型是解决该疾病病理机制的关键。在这里，我们概述了单核细胞和巨噬细胞在稳态和病毒感染中的现有知识，并总结了它们在COVID-19中作用的概念和关键发现。虽然中度COVID-19患者血液中的单核细胞呈现出炎症性、干扰素刺激基因（ISG）驱动的表型，但以HLA-DR表达缺失和S100 alarmin表达诱导为缩影的细胞功能障碍是其在重度疾病中的主要特征。源自浸润性炎性单核细胞的COVID-19中的肺巨噬细胞处于超活化状态，导致促炎细胞因子释放和细胞毒性效应细胞募集的有害循环，从而加剧感染部位的组织损伤。
COVID-19 is a contagious viral disease caused by SARS-CoV-2 that led to an ongoing pandemic with massive global health and socioeconomic consequences. The disease is characterized primarily, but not exclusively, by respiratory clinical manifestations ranging from mild common cold symptoms, including cough and fever, to severe respiratory distress and multi-organ failure. Macrophages, a heterogeneous group of yolk-sac derived, tissue-resident mononuclear phagocytes of complex ontogeny present in all mammalian organs, play critical roles in developmental, homeostatic and host defense processes with tissue-dependent plasticity. In case of infection, they are responsible for early pathogen recognition, initiation and resolution of inflammation, as well as repair of tissue damage. Monocytes, bone-marrow derived blood-resident phagocytes, are recruited under pathological conditions such as viral infections to the affected tissue to defend the organism against invading pathogens and to aid in efficient resolution of inflammation. Given their pivotal function in host defense and the potential danger posed by their dysregulated hyperinflammation, understanding monocyte and macrophage phenotypes in COVID-19 is key for tackling the disease’s pathological mechanisms. Here, we outline current knowledge on monocytes and macrophages in homeostasis and viral infections and summarize concepts and key findings on their role in COVID-19. While monocytes in the blood of patients with moderate COVID-19 present with an inflammatory, interferon-stimulated gene (ISG)-driven phenotype, cellular dysfunction epitomized by loss of HLA-DR expression and induction of S100 alarmin expression is their dominant feature in severe disease. Pulmonary macrophages in COVID-19 derived from infiltrating inflammatory monocytes are in a hyperactivated state resulting in a detrimental loop of pro-inflammatory cytokine release and recruitment of cytotoxic effector cells thereby exacerbating tissue damage at the site of infection.
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DOI：
10.1126/science.abd3072
发表时间：
2020-11-13
期刊：
Science (New York, N.Y.)
影响因子：
--
作者：
Daly JL;Simonetti B;Klein K;Chen KE;Williamson MK;Antón-Plágaro C;Shoemark DK;Simón-Gracia L;Bauer M;Hollandi R;Greber UF;Horvath P;Sessions RB;Helenius A;Hiscox JA;Teesalu T;Matthews DA;Davidson AD;Collins BM;Cullen PJ;Yamauchi Y
通讯作者：
Yamauchi Y
影响因子：
7.3
作者：
Baharom F;Rankin G;Blomberg A;Smed-Sörensen A
通讯作者：
Smed-Sörensen A
影响因子：
12.3
作者：
Aschenbrenner AC;Mouktaroudi M;Krämer B;Oestreich M;Antonakos N;Nuesch-Germano M;Gkizeli K;Bonaguro L;Reusch N;Baßler K;Saridaki M;Knoll R;Pecht T;Kapellos TS;Doulou S;Kröger C;Herbert M;Holsten L;Horne A;Gemünd ID;Rovina N;Agrawal S;Dahm K;van Uelft M;Drews A;Lenkeit L;Bruse N;Gerretsen J;Gierlich J;Becker M;Händler K;Kraut M;Theis H;Mengiste S;De Domenico E;Schulte-Schrepping J;Seep L;Raabe J;Hoffmeister C;ToVinh M;Keitel V;Rieke G;Talevi V;Skowasch D;Aziz NA;Pickkers P;van de Veerdonk FL;Netea MG;Schultze JL;Kox M;Breteler MMB;Nattermann J;Koutsoukou A;Giamarellos-Bourboulis EJ;Ulas T;German COVID-19 Omics Initiative (DeCOI)
通讯作者：
German COVID-19 Omics Initiative (DeCOI)
影响因子：
5
作者：
Desforges M;Miletti TC;Gagnon M;Talbot PJ
通讯作者：
Talbot PJ
影响因子：
15.9
作者：
Fadok, VA;Bratton, DL;Henson, PM
通讯作者：
Henson, PM