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重度联合免疫缺陷(SCID)小鼠中的沙眼衣原体肺炎

Chlamydia trachomatis pneumonia in the severe combined immunodeficiency (SCID) mouse.

作者信息

Magee D M, Igietseme J U, Smith J G, Bleicker C A, Grubbs B G, Schachter J, Rank R G, Williams D M

机构信息

Department of Research Immunology, San Antonio State Chest Hospital, TX 78223.

出版信息

Reg Immunol. 1993 Nov-Dec;5(6):305-11.

PMID:7520728
Abstract

We have developed a model of pneumonia caused by the mouse pneumonitis agent (MoPn, murine Chlamydia trachomatis) in the C.B-17 severe combined immunodeficiency (SCID) mouse. In contrast to our prior models in the nude athymic (nu/nu) and heterozygous (nu/+) mouse, SCID mice lack B-cell function and gamma delta T-cell function. SCID mice were more susceptible to MoPn than nu/nu or nu/+ mice both by criteria of mortality and quantitative lung culture. SCID mice could be reconstituted with thymocytes to be more resistant to MoPn (in the absence of significant antibody production), but the protection was modest and less than that in T-cell reconstituted nu/nu mice in our previous studies. A nu/+ MoPn-specific T-cell clone with a Th1-like cytokine profile also provided modest but significant protection without significant antibody production. The SCID mouse is a useful model to study T-cell-mediated immunity to MoPn in a B cell and gamma delta T-cell-deficient environment.

摘要

我们已经在C.B-17严重联合免疫缺陷(SCID)小鼠中建立了由小鼠肺炎病原体(MoPn,鼠沙眼衣原体)引起的肺炎模型。与我们之前在裸无胸腺(nu/nu)和杂合(nu/+)小鼠中建立的模型不同,SCID小鼠缺乏B细胞功能和γδT细胞功能。无论是依据死亡率还是定量肺培养标准,SCID小鼠比nu/nu或nu/+小鼠对MoPn更易感。SCID小鼠可用胸腺细胞进行重建,从而对MoPn更具抗性(在无显著抗体产生的情况下),但这种保护作用适中,且低于我们之前研究中T细胞重建的nu/nu小鼠。一个具有Th1样细胞因子谱的nu/+ MoPn特异性T细胞克隆在无显著抗体产生的情况下也提供了适度但显著的保护作用。SCID小鼠是一种有用的模型,可用于在B细胞和γδT细胞缺陷的环境中研究T细胞介导的对MoPn的免疫。

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