Increased interleukin-10 expression is not responsible for failure of T helper 1 immunity to resolve airborne Mycobacterium tuberculosis infection in mice
Increased interleukin-10 expression is not responsible for failure of T helper 1 immunity to resolve airborne Mycobacterium tuberculosis infection in mice
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DOI：
10.1046/j.1365-2567.2003.01645.x
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发表时间：
2003-06-01
期刊：
影响因子：
6.4
通讯作者：
North, RJ
中科院分区：
文献类型：
--
作者：
Jung, YJ;Ryan, L;North, RJ
为了确定小鼠是否无法解析结核分枝杆菌（MTB）感染是由于白介素（IL）-10对T辅助1（Th1）免疫下调的结果，将其与IL-10基因删除的小鼠进行了比较野生型（WT）小鼠在制造IL-10 mRNA的能力方面产生Th1介导的免疫力[AS通过合成mRNA的干扰素 - γ（IFN-GAMMA）]，IL-12P40和诱导型一氧化氮合酶（INOS）和控制肺部感染来测量。发现WT小鼠对感染的反应包括肺中IL-10 mRNA合成的大幅度和持续增加。 WT和IL-10（ - / - ）小鼠的肺中的Th1反应通过IFN-Gamma，IL-12P40和Inos的mRNA的合成大量而持续增加，并且这些mRNA物种的水平较高，证明在IL-10（ - / - ）小鼠的肺中制成，尤其是在感染的早期阶段。但是，IL-10（ - / - ）小鼠的能力并不比WT小鼠打击感染。
With a view to determining whether failure of mice to resolve Mycobacterium tuberculosis (Mtb) infection is a consequence of downregulation of T helper 1 (Th1) immunity by interleukin (IL)-10, mice deleted of the gene for IL-10 were compared with wild-type (WT) mice in terms of their ability to make IL-10 mRNA, generate Th1-mediated immunity [as measured by synthesis of mRNA for interferon-gamma (IFN-gamma)], IL-12p40 and inducible nitric oxide synthase (iNOS), and to control lung infection. It was found that the response of WT mice to infection included a substantial and sustained increase in IL-10 mRNA synthesis in the lungs. A Th1 response in the lungs of WT and IL-10(-/-) mice was evidenced by a large and sustained increase in the synthesis of mRNA for IFN-gamma, IL-12p40 and iNOS, with somewhat higher levels of these mRNA species being made in the lungs of IL-10(-/-) mice, particularly at an early stage of infection. However, IL-10(-/-) mice were no more capable than WT mice at combating infection.