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树突状细胞耗竭与功能障碍:深入了解 SARS-CoV-2 感染。

Depletion and Dysfunction of Dendritic Cells: Understanding SARS-CoV-2 Infection.

机构信息

Division of Trauma & Surgical Critical Care, Department of Surgery, Tongji Hospital, Tongji, China.

Department of Immunology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.

出版信息

Front Immunol. 2022 Feb 21;13:843342. doi: 10.3389/fimmu.2022.843342. eCollection 2022.

Abstract

Uncontrolled severe acute respiratory syndrome-coronavirus (SARS-CoV)-2 infection is closely related to disorders of the innate immune and delayed adaptive immune systems. Dendritic cells (DCs) "bridge" innate immunity and adaptive immunity. DCs have important roles in defending against SARS-CoV-2 infection. In this review, we summarize the latest research concerning the role of DCs in SARS-CoV-2 infection. We focus on the complex interplay between DCs and SARS-CoV-2: pyroptosis-induced activation; activation of the renin-angiotensin-aldosterone system; and activation of dendritic cell-specific intercellular adhesion molecule 3-grabbing non-integrin. We also discuss the decline in DC number, the impaired antigen-presentation capability, and the reduced production of type-I interferon of DCs in severe SARS-CoV-2 infection. In addition, we discuss the potential mechanisms for pathological activation of DCs to understand the pattern of SARS-CoV-2 infection. Lastly, we provide a brief overview of novel vaccination and immunotherapy strategies based on DC targeting to overcome SARS-CoV-2 infection.

摘要

未控制的严重急性呼吸综合征冠状病毒 2 型(SARS-CoV-2)感染与固有免疫和迟发性适应性免疫系统紊乱密切相关。树突状细胞(DCs)“连接”固有免疫和适应性免疫。DCs 在抵抗 SARS-CoV-2 感染方面发挥着重要作用。在这篇综述中,我们总结了有关 DCs 在 SARS-CoV-2 感染中的作用的最新研究。我们重点讨论了 DCs 与 SARS-CoV-2 之间的复杂相互作用:细胞焦亡诱导的激活;肾素-血管紧张素-醛固酮系统的激活;和树突状细胞特异性细胞间黏附分子 3 抓取非整联蛋白的激活。我们还讨论了严重 SARS-CoV-2 感染中 DC 数量下降、抗原呈递能力受损以及Ⅰ型干扰素产生减少的问题。此外,我们还讨论了 DC 病理性激活的潜在机制,以了解 SARS-CoV-2 感染的模式。最后,我们简要概述了基于针对 DC 的新型疫苗接种和免疫治疗策略,以克服 SARS-CoV-2 感染。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bcd7/8898834/7a070cae535c/fimmu-13-843342-g001.jpg

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