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抗 SARS-CoV-2 抗体控制 SARS-CoV-2 感染引起的补体炎症反应。

Control of complement-induced inflammatory responses to SARS-CoV-2 infection by anti-SARS-CoV-2 antibodies.

机构信息

Department of Experimental Immunology, Amsterdam UMC location AMC, Amsterdam, The Netherlands.

Amsterdam Institute for Infection and Immunity, Infectious Diseases, Amsterdam, The Netherlands.

出版信息

EMBO J. 2024 Apr;43(7):1135-1163. doi: 10.1038/s44318-024-00061-0. Epub 2024 Feb 28.

DOI:10.1038/s44318-024-00061-0
PMID:38418557
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10987522/
Abstract

Dysregulated immune responses contribute to the excessive and uncontrolled inflammation observed in severe COVID-19. However, how immunity to SARS-CoV-2 is induced and regulated remains unclear. Here, we uncover the role of the complement system in the induction of innate and adaptive immunity to SARS-CoV-2. Complement rapidly opsonizes SARS-CoV-2 particles via the lectin pathway. Complement-opsonized SARS-CoV-2 efficiently induces type-I interferon and pro-inflammatory cytokine responses via activation of dendritic cells, which are inhibited by antibodies against the complement receptors (CR) 3 and 4. Serum from COVID-19 patients, or monoclonal antibodies against SARS-CoV-2, attenuate innate and adaptive immunity induced by complement-opsonized SARS-CoV-2. Blocking of CD32, the FcγRII antibody receptor of dendritic cells, restores complement-induced immunity. These results suggest that opsonization of SARS-CoV-2 by complement is involved in the induction of innate and adaptive immunity to SARS-CoV-2 in the acute phase of infection. Subsequent antibody responses limit inflammation and restore immune homeostasis. These findings suggest that dysregulation of the complement system and FcγRII signaling may contribute to severe COVID-19.

摘要

失调的免疫反应导致了严重 COVID-19 中观察到的过度和失控的炎症。然而，人们对 SARS-CoV-2 免疫的诱导和调节仍不清楚。在这里，我们揭示了补体系统在诱导 SARS-CoV-2 的先天和适应性免疫中的作用。补体通过凝集素途径迅速调理 SARS-CoV-2 颗粒。补体调理的 SARS-CoV-2 通过激活树突状细胞有效地诱导 I 型干扰素和促炎细胞因子反应，而补体受体（CR）3 和 4 的抗体对此反应具有抑制作用。COVID-19 患者的血清或针对 SARS-CoV-2 的单克隆抗体可减弱补体调理 SARS-CoV-2 诱导的先天和适应性免疫。阻断树突状细胞的 FcγRII 抗体受体 CD32 可恢复补体诱导的免疫。这些结果表明，补体对 SARS-CoV-2 的调理作用参与了感染急性期 SARS-CoV-2 的先天和适应性免疫的诱导。随后的抗体反应限制了炎症并恢复了免疫稳态。这些发现表明补体系统和 FcγRII 信号的失调可能导致严重的 COVID-19。

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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77b6/10987522/b9fb897e712f/44318_2024_61_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77b6/10987522/a1858b4f714b/44318_2024_61_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77b6/10987522/ae7f87bbdee3/44318_2024_61_Fig7_ESM.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77b6/10987522/e8846aa99ebd/44318_2024_61_Fig8_ESM.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77b6/10987522/33aaf39ed120/44318_2024_61_Fig9_ESM.jpg
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