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将来自感染微小隐孢子虫的干扰素-γ和白细胞介素-12缺陷小鼠的保护性免疫过继转移给未感染的受体。

Adoptive transfer of protective immunity from Cryptosporidium parvum-infected interferon-gamma and interleukin-12-deficient mice to naive recipients.

作者信息

Tessema Tesfaye Sisay, Dauber Elke, Petry Franz

机构信息

Institute of Medical Microbiology and Hygiene, University Medical Center, Johannes Gutenberg-University Mainz, Augustusplatz/Hochhaus, D-55131 Mainz, Germany.

出版信息

Vaccine. 2009 Nov 5;27(47):6575-81. doi: 10.1016/j.vaccine.2009.08.036. Epub 2009 Aug 28.

Abstract

We investigated the possibility of transfer immunity from Cryptosporidium parvum-infected interferon-gamma (GKO) and interleukin-12p40 (IL-12KO) deficient C57BL/6 mice to naive mice by transfer of intraepithelial lymphocytes (IELs) and CD4(+) T cells from spleen and mesenteric lymph nodes (MLNs). Three days after the transfer recipients were infected with C. parvum. IELs isolated from GKO donor mice after resolution of infection (day 15) but not at the peak of infection (day 8) significantly reduced the parasite load in recipient mice. In IL-12KO mice, IELs and also CD4(+) T cells isolated from the spleen and MLNs of donor mice at the peak of infection (day 5) and after resolution (day 15) significantly reduced the parasite excretion, emphasizing the role of interferon-gamma in the host-parasite interaction. However, after resolution of infection, interferon-gamma-independent mechanisms have evolved that render GKO IELs capable of protecting mice from severe infection.

摘要

我们研究了通过转移上皮内淋巴细胞(IELs)以及来自脾脏和肠系膜淋巴结(MLNs)的CD4(+) T细胞,将感染微小隐孢子虫的干扰素-γ(GKO)缺陷和白细胞介素-12p40(IL-12KO)缺陷的C57BL/6小鼠的免疫转移给未感染小鼠的可能性。转移三天后,受体小鼠感染微小隐孢子虫。从感染消退后(第15天)而非感染高峰期(第8天)的GKO供体小鼠分离的IELs显著降低了受体小鼠体内的寄生虫负荷。在IL-12KO小鼠中,从感染高峰期(第5天)和消退后(第15天)的供体小鼠脾脏和MLNs分离的IELs以及CD4(+) T细胞显著减少了寄生虫排泄,这强调了干扰素-γ在宿主-寄生虫相互作用中的作用。然而,感染消退后,不依赖干扰素-γ的机制已经形成,使GKO IELs能够保护小鼠免受严重感染。

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