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沙门氏菌特异性抗体的结合通过增强巨噬细胞对细菌的摄取和诱导细胞凋亡来促进特异性 T 细胞应答。

Binding of Salmonella-specific antibody facilitates specific T cell responses via augmentation of bacterial uptake and induction of apoptosis in macrophages.

机构信息

Laboratory of Immunoregulation, Kitasato Institute for Life Sciences and Graduate School of Infection Control Sciences, Kitasato University, Tokyo, Japan.

出版信息

J Infect Dis. 2010 Jan 1;201(1):62-70. doi: 10.1086/648615.

DOI:10.1086/648615
PMID:19929376
Abstract

BACKGROUND

Most antigens from intracellular bacteria or vaccines induce both humoral and cell-mediated immune responses, but interactions between these responses are not fully understood. This study aims to resolve how specific antibodies participate in the activation of specific T cells in protecting hosts against Salmonella enterica serotype Typhimurium (S. typhimurium) infection.

METHODS

Mice were administered anti-Salmonella immunoglobulin G (IgG) 1 day before Salmonella infection, and survival rate was observed. For in vitro assay, Salmonella bacteria were treated with anti-Salmonella IgG or control IgG before infection of the RAW264.7 or HEp2 cells. After infection, cell-associated bacteria number, induction of apoptosis, and production of nitric oxide were examined. In addition, antigen presentation assays using Salmonella-primed T cells were performed.

RESULTS

Treatment of S. typhimurium with anti-Salmonella IgG enhanced the macrophages' uptake of bacteria and induced high-frequency apoptotic cell death. In vitro antigen presentation assay revealed that the extracellular vesicles isolated from apoptotic cells caused by infection with anti-Salmonella IgG-treated S. typhimurium facilitated the responses of Salmonella-specific T cells.

CONCLUSION

Our findings suggest that humoral immunity cooperates with cell-mediated immunity upon induction of apoptosis in host cells to establish protective immunity against Salmonella infection, even if it does not directly eliminate intracellular microorganisms.

摘要

背景

大多数来自细胞内细菌或疫苗的抗原既能诱导体液免疫反应,也能诱导细胞免疫反应,但这些反应之间的相互作用尚未完全阐明。本研究旨在解决特定抗体如何参与激活特定 T 细胞,以保护宿主免受鼠伤寒沙门氏菌(S. typhimurium)感染。

方法

在沙门氏菌感染前一天给小鼠注射抗沙门氏菌 IgG,观察存活率。为了进行体外试验,用抗沙门氏菌 IgG 或对照 IgG 处理沙门氏菌,然后感染 RAW264.7 或 HEp2 细胞。感染后,检测细胞相关细菌数量、细胞凋亡诱导和一氧化氮产生情况。此外,还进行了使用经沙门氏菌致敏的 T 细胞的抗原呈递试验。

结果

用抗沙门氏菌 IgG 处理鼠伤寒沙门氏菌可增强巨噬细胞对细菌的摄取,并诱导高频细胞凋亡。体外抗原呈递试验显示,用抗沙门氏菌 IgG 处理的 S. typhimurium 感染导致的细胞凋亡所分离的细胞外囊泡促进了沙门氏菌特异性 T 细胞的反应。

结论

我们的研究结果表明,即使不能直接消除细胞内微生物,体液免疫也能与细胞免疫协同作用,在宿主细胞诱导凋亡的情况下建立对沙门氏菌感染的保护性免疫。

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