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T淋巴细胞介导小鼠对小肠结肠炎耶尔森菌的保护作用:对小肠结肠炎耶尔森菌特异性鼠T细胞克隆的特性研究

T lymphocytes mediate protection against Yersinia enterocolitica in mice: characterization of murine T-cell clones specific for Y. enterocolitica.

作者信息

Autenrieth I B, Tingle A, Reske-Kunz A, Heesemann J

机构信息

Institute for Hygiene and Microbiology, University of Würzburg, Germany.

出版信息

Infect Immun. 1992 Mar;60(3):1140-9. doi: 10.1128/iai.60.3.1140-1149.1992.

DOI:10.1128/iai.60.3.1140-1149.1992
PMID:1541529
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC257605/
Abstract

Yersinia enterocolitica is enteropathogenic for humans and rodents, causing intestinal and extraintestinal diseases. The cellular immune response of the infected host has not yet been analyzed in detail. Therefore, we used a parenteral mouse infection model to determine the role of T lymphocytes in immunity against Y. enterocolitica. We report the generation and characterization of Y. enterocolitica-specific T-cell clones isolated from spleens of intravenously infected C57BL/6 mice. The T-cell clones obtained showed the phenotype of helper T cells (L3T4) or cytotoxic T cells (Lyt2). All T-cell clones were positive for the interleukin-2 (IL-2) receptor (Tac antigen, p55 subunit) and were negative for the gamma delta T-cell receptor. L3T4+ clones produced small quantities of IL-2 (less than 1 U/ml) when stimulated with heat-killed Y. enterocolitica, whereas Lyt2+ clones produced no or extremely low levels of IL-2. In contrast to IL-2 production, both L3T4+ and Lyt2+ T-cell clones produced considerable quantities of gamma interferon (500 U/ml). When transferred into nonimmune mice, some of the L3T4+, as well as the Lyt2+, T-cell clones could mediate at least partial protection against a challenge of a lethal dose of Y. enterocolitica. These data demonstrate for the first time the generation and characterization of Y. enterocolitica-specific T-cell clones and provide evidence that T cells may be involved in protection against enteropathogenic Y. enterocolitica.

摘要

小肠结肠炎耶尔森菌对人类和啮齿动物具有肠道致病性,可引起肠道和肠道外疾病。尚未对受感染宿主的细胞免疫反应进行详细分析。因此,我们使用了一种肠胃外小鼠感染模型来确定T淋巴细胞在抗小肠结肠炎耶尔森菌免疫中的作用。我们报告了从小肠结肠炎耶尔森菌静脉感染的C57BL/6小鼠脾脏中分离出的小肠结肠炎耶尔森菌特异性T细胞克隆的产生和特性。获得的T细胞克隆表现出辅助性T细胞(L3T4)或细胞毒性T细胞(Lyt2)的表型。所有T细胞克隆的白细胞介素-2(IL-2)受体(Tac抗原,p55亚基)呈阳性,γδT细胞受体呈阴性。用热灭活的小肠结肠炎耶尔森菌刺激时,L3T4+克隆产生少量IL-2(低于1 U/ml),而Lyt2+克隆不产生或产生极低水平的IL-2。与IL-2产生情况相反,L3T4+和Lyt2+T细胞克隆均产生大量γ干扰素(500 U/ml)。当将一些L3T4+以及Lyt2+T细胞克隆转移到未免疫的小鼠中时,它们可以介导至少部分抵抗致死剂量小肠结肠炎耶尔森菌攻击的保护作用。这些数据首次证明了小肠结肠炎耶尔森菌特异性T细胞克隆的产生和特性,并提供了T细胞可能参与抵抗肠道致病性小肠结肠炎耶尔森菌保护作用的证据。

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Control of early Salmonella typhimurium growth in innately Salmonella-resistant mice does not require functional T lymphocytes.在天生对鼠伤寒沙门氏菌有抗性的小鼠中,控制早期鼠伤寒沙门氏菌的生长不需要功能性T淋巴细胞。
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