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体液免疫受抑制与登革热非结构蛋白 NS1 诱导的抗死亡受体抗体片段在小鼠中有关。

Suppressed humoral immunity is associated with dengue nonstructural protein NS1-elicited anti-death receptor antibody fractions in mice.

机构信息

Department of Molecular Biology and Human Genetics, Tzu-Chi University, Hualien, Taiwan.

Department of Experimental Immunology, Institute of Development, Aging and Cancer, Tohoku University, Sendai, Japan.

出版信息

Sci Rep. 2020 Apr 14;10(1):6294. doi: 10.1038/s41598-020-62958-0.

DOI:10.1038/s41598-020-62958-0
PMID:32286343
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7156414/
Abstract

Dengue virus (DENV) infections may cause life-threatening dengue hemorrhagic fever (DHF). Suppressed protective immunity was shown in these patients. Although several hypotheses have been formulated, the mechanism of DENV-induced immunosuppression remains unclear. Previously, we found that cross-reactive antibodies against tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) receptor 1 (death receptor 4 [DR4]) were elicited in DHF patients, and that anti-DR4 autoantibody fractions were elicited by nonstructural protein 1 (NS1) immunizations in experimental mice. In this study, we found that anti-DR4 antibodies could suppress B lymphocyte function in vitro and in vivo. Treatment with the anti-DR4 immunoglobulin (Ig) induced caspase-dependent cell death in immortalized B lymphocyte Raji cells in vitro. Anti-DR4 Igs elicited by NS1 and DR4 immunizations markedly suppressed mouse spleen transitional T2 B (IgMIgD), bone marrow pre-pro-B (B220CD43), pre-B (B220CD43), and mature B cell (B220IgD) subsets in mice. Furthermore, functional analysis revealed that the pre-elicitation of anti-NS1 and anti-DR4 Ig titers suppressed subsequently neutralizing antibody production by immunization with DENV envelop protein. Our data suggest that the elicitation of anti-DR4 titers through DENV NS1 immunization plays a suppressive role in humoral immunity in mice.

摘要

登革热病毒（DENV）感染可能导致危及生命的登革出血热（DHF）。这些患者表现出保护性免疫抑制。尽管已经提出了几种假说，但 DENV 诱导免疫抑制的机制仍不清楚。先前，我们发现登革热患者中产生了针对肿瘤坏死因子相关凋亡诱导配体（TRAIL）受体 1（死亡受体 4 [DR4]）的交叉反应性抗体，并且实验小鼠中通过非结构蛋白 1（NS1）免疫接种产生了抗-DR4 自身抗体片段。在这项研究中，我们发现抗-DR4 抗体可以在体外和体内抑制 B 淋巴细胞功能。在体外，用抗-DR4 免疫球蛋白（Ig）处理可诱导永生化 B 淋巴细胞 Raji 细胞中的 caspase 依赖性细胞死亡。通过 NS1 和 DR4 免疫接种产生的抗-DR4 Ig 可显著抑制小鼠脾脏过渡性 T2 B（IgM+IgD）、骨髓前前 B（B220+CD43）、前 B（B220+CD43）和成熟 B 细胞（B220+IgD）亚群。此外，功能分析表明，抗-NS1 和抗-DR4 Ig 滴度的预先产生抑制了随后用 DENV 包膜蛋白免疫接种产生的中和抗体产生。我们的数据表明，通过 DENV NS1 免疫接种产生抗-DR4 滴度在小鼠的体液免疫中起抑制作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dd1c/7156414/6c673dfd4169/41598_2020_62958_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dd1c/7156414/595aa56c98f9/41598_2020_62958_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dd1c/7156414/dd68733ba24a/41598_2020_62958_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dd1c/7156414/d1a8ed64b4f0/41598_2020_62958_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dd1c/7156414/b3094410c6a7/41598_2020_62958_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dd1c/7156414/37b7b8c6f3db/41598_2020_62958_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dd1c/7156414/cc5df2a67e72/41598_2020_62958_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dd1c/7156414/6c673dfd4169/41598_2020_62958_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dd1c/7156414/595aa56c98f9/41598_2020_62958_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dd1c/7156414/dd68733ba24a/41598_2020_62958_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dd1c/7156414/d1a8ed64b4f0/41598_2020_62958_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dd1c/7156414/b3094410c6a7/41598_2020_62958_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dd1c/7156414/37b7b8c6f3db/41598_2020_62958_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dd1c/7156414/cc5df2a67e72/41598_2020_62958_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dd1c/7156414/6c673dfd4169/41598_2020_62958_Fig7_HTML.jpg

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