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感染减毒变异细胞的T细胞耗竭小鼠原发性念珠菌病的病程

Course of primary candidiasis in T cell-depleted mice infected with attenuated variant cells.

作者信息

Romani L, Mencacci A, Cenci E, Mosci P, Vitellozzi G, Grohmann U, Puccetti P, Bistoni F

机构信息

Department of Experimental Medicine and Biochemical Sciences, University of Perugia, Italy.

出版信息

J Infect Dis. 1992 Dec;166(6):1384-92. doi: 10.1093/infdis/166.6.1384.

Abstract

Anti-CD4, anti-CD8, or anti-interferon-gamma (IFN-gamma) antibodies or combinations of them were administered in the early stages of chronic infection of mice with a Candida albicans live vaccine strain, and the animals were monitored for course of primary infection, development of delayed-type hypersensitivity, resistance to reinfection, production of interleukin 2 (IL-2) and IFN-gamma in vitro by splenic lymphocytes, and levels of IL-2 and IFN-gamma transcripts in these cells. CD4+ cell and IFN-gamma depletion resulted in the development of fatal candidiasis by the attenuated yeast vaccine. In contrast, either treatment alone modified the course but not the outcome of primary infection, though each prevented the development of resistance to reinfection. Our data thus indicate that both IFN-gamma and CD4+ cells participate in resistance to primary infection with attenuated yeast cells and are critical in the induction of persistent systemic anticandidal immunity.

摘要

在小鼠被白色念珠菌活疫苗株慢性感染的早期阶段,给予抗CD4、抗CD8或抗γ干扰素(IFN-γ)抗体或它们的组合,然后监测这些动物原发性感染的病程、迟发型超敏反应的发展、对再感染的抵抗力、脾淋巴细胞在体外产生白细胞介素2(IL-2)和IFN-γ的情况,以及这些细胞中IL-2和IFN-γ转录本的水平。CD4 + 细胞和IFN-γ的耗竭导致减毒酵母疫苗引发致命的念珠菌病。相比之下,单独的任何一种治疗虽改变了原发性感染的病程,但未改变其结果,不过每种治疗都阻止了对再感染抵抗力的发展。因此,我们的数据表明,IFN-γ和CD4 + 细胞都参与了对减毒酵母细胞原发性感染的抵抗力,并且在诱导持续性全身抗念珠菌免疫中起关键作用。

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