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CD8基因敲除小鼠通过接种WR201(一种减毒活的羊种布鲁氏菌突变株)而受到保护,免受攻击。

CD8 knockout mice are protected from challenge by vaccination with WR201, a live attenuated mutant of Brucella melitensis.

作者信息

Yingst Samuel L, Izadjoo Mina, Hoover David L

机构信息

Department of Bacterial Diseases, Walter Reed Army Institute of Research, Silver Spring, MD 20910-5100, USA ; Armed Forces Research Institute of Medical Sciences, 315/6 Rajvithi, Bangkok 10400, Thailand.

出版信息

Clin Dev Immunol. 2013;2013:686919. doi: 10.1155/2013/686919. Epub 2013 Oct 28.

Abstract

CD8+ T cells have been reported to play an important role in defense against B. abortus infection in mouse models. In the present report, we use CD8 knockout mice to further elucidate the role of these cells in protection from B. melitensis infection. Mice were immunized orally by administration of B. melitensis WR201, a purine auxotrophic attenuated vaccine strain, then challenged intranasally with B. melitensis 16M. In some experiments, persistence of WR201 in the spleens of CD8 knockout mice was slightly longer than that in the spleens of normal mice. However, development of anti-LPS serum antibody, antigen-induced production of γ-interferon (IFN-γ) by immune splenic lymphocytes, protection against intranasal challenge, and recovery of nonimmunized animals from intranasal challenge were similar between normal and knockout animals. Further, primary Brucella infection was not exacerbated in perforin knockout and Fas-deficient mice and these animals' anti-Brucella immune responses were indistinguishable from those of normal mice. These results indicate that CD8+ T cells do not play an essential role as either cytotoxic cells or IFN-γ producers, yet they do participate in a specific immune response to immunization and challenge in this murine model of B. melitensis infection.

摘要

据报道,在小鼠模型中,CD8 + T细胞在抵御流产布鲁氏菌感染中发挥重要作用。在本报告中,我们使用CD8基因敲除小鼠进一步阐明这些细胞在抵抗羊种布鲁氏菌感染中的作用。通过口服给予嘌呤营养缺陷型减毒疫苗株羊种布鲁氏菌WR201对小鼠进行免疫,然后经鼻用羊种布鲁氏菌16M进行攻击。在一些实验中,WR201在CD8基因敲除小鼠脾脏中的持续时间略长于正常小鼠脾脏中的持续时间。然而,正常动物和基因敲除动物在抗LPS血清抗体的产生、免疫脾淋巴细胞抗原诱导的γ干扰素(IFN-γ)产生、抵御经鼻攻击的能力以及未免疫动物从经鼻攻击中恢复的情况方面相似。此外,穿孔素基因敲除小鼠和Fas缺陷小鼠的原发性布鲁氏菌感染并未加剧,并且这些动物的抗布鲁氏菌免疫反应与正常小鼠的无法区分。这些结果表明,CD8 + T细胞作为细胞毒性细胞或IFN-γ产生细胞并不发挥关键作用,但它们确实参与了在这种羊种布鲁氏菌感染小鼠模型中针对免疫和攻击的特异性免疫反应。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b0ea/3830850/b4f0e1c1abe6/CDI2013-686919.001.jpg

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