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白细胞介素-12增强BALB/c小鼠对结核分枝杆菌感染的抵抗力。

IL-12 increases resistance of BALB/c mice to Mycobacterium tuberculosis infection.

作者信息

Flynn J L, Goldstein M M, Triebold K J, Sypek J, Wolf S, Bloom B R

机构信息

Howard Hughes Medical Institute, Albert Einstein College of Medicine, Bronx, NY 10461, USA.

出版信息

J Immunol. 1995 Sep 1;155(5):2515-24.

PMID:7650381
Abstract

IL-12, a cytokine produced by macrophages and B cells, has recently been found to exert pleiotropic effects on the immune system. When BALB/c mice, a strain highly susceptible to virulent Mycobacterium tuberculosis infection, were given IL-12 at the initiation of infection with M. tuberculosis, their mean survival time doubled from 58 to 112 days. IL-12-treated mice had diminished bacterial burdens, whereas treatment with exogenous IFN-gamma had no effect on survival or bacterial burden. IL-12 treatment also delayed lung pathology in BALB/c mice. In contrast with the findings in the BALB/c model, IL-12 did not increase survival of M. tuberculosis-infected gko mice, transgenic mice in which the IFN-gamma gene has been disrupted, indicating that IL-12 does not induce protection against tuberculosis in mice in the absence of IFN-gamma.

摘要

白细胞介素-12(IL-12)是一种由巨噬细胞和B细胞产生的细胞因子,最近发现它对免疫系统具有多效性作用。当对高度易感染强毒力结核分枝杆菌的BALB/c小鼠在感染结核分枝杆菌开始时给予IL-12,它们的平均存活时间从58天翻倍至112天。经IL-12处理的小鼠细菌负荷减少,而用外源性干扰素-γ(IFN-γ)处理对存活或细菌负荷没有影响。IL-12处理还延缓了BALB/c小鼠的肺部病变。与BALB/c模型中的发现相反,IL-12并没有提高结核分枝杆菌感染的银杏小鼠(IFN-γ基因已被破坏的转基因小鼠)的存活率,这表明在没有IFN-γ的情况下,IL-12不会诱导小鼠对结核病产生保护作用。

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