Interleukin 12 (IL-12) is crucial to the development of protective immunity in mice intravenously infected with mycobacterium tuberculosis.
Interleukin 12 (IL-12) is crucial to the development of protective immunity in mice intravenously infected with mycobacterium tuberculosis.
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DOI：
10.1084/jem.186.1.39
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发表时间：
1997-07-07
影响因子：
15.3
通讯作者：
Orme, IM
中科院分区：
文献类型：
--
作者：
Cooper, AM;Magram, J;Ferrante, J;Orme, IM
对结核分枝杆菌感染的免疫与分泌细胞因子的保护性CD 4 T细胞的出现相关，导致巨噬细胞的活化和单核细胞的募集以启动肉芽肿形成。介导巨噬细胞激活的细胞因子是干扰素-γ（IFN-γ），其诱导很大程度上依赖于白细胞介素-12（IL-12）。为了阐明IL-12在结核免疫中的作用，将IL-12 p40−/−小鼠感染M.结核病和它们控制细菌生长的能力以及它们免疫应答的其他特征。IL-12 p40-/-小鼠无法控制细菌生长，这似乎与缺乏先天性和获得性IFN-γ来源有关。在IL-12 p40−/−小鼠中，通过迟发型超敏反应和感染部位淋巴细胞蓄积测量的T细胞活化均显著降低。因此，IL-12对于产生针对M的保护性免疫应答是必需的。结核病，其主要功能是诱导IFN-γ的表达和激活能够产生保护性肉芽肿的抗原特异性淋巴细胞。
Immunity to Mycobacterium tuberculosis infection is associated with the emergence of protective CD4 T cells that secrete cytokines, resulting in activation of macrophages and the recruitment of monocytes to initiate granuloma formation. The cytokine-mediating macrophage activation is interferon-γ (IFN-γ), which is largely dependent on interleukin-12 (IL-12) for its induction. To address the role of IL-12 in immunity to tuberculosis, IL-12 p40−/− mice were infected with M. tuberculosis and their capacity to control bacterial growth and other characteristics of their immune response were determined. The IL-12 p40−/− mice were unable to control bacterial growth and this appeared to be linked to the absence of both innate and acquired sources of IFN-γ. T cell activation as measured by delayed type hypersensitivity and lymphocyte accumulation at the site of infection were both markedly reduced in the IL-12 p40−/− mice. Therefore, IL-12 is essential to the generation of a protective immune response to M. tuberculosis, with its main functions being the induction of the expression of IFN-γ and the activation of antigen-specific lymphocytes capable of creating a protective granuloma.
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DOI：
10.1084/jem.177.4.1199
发表时间：
1993-04-01
期刊：
The Journal of experimental medicine
影响因子：
--
作者：
Manetti R;Parronchi P;Giudizi MG;Piccinni MP;Maggi E;Trinchieri G;Romagnani S
通讯作者：
Romagnani S
影响因子：
64.8
作者：
Austrup, F;Vestweber, D;Hamann, A
通讯作者：
Hamann, A
影响因子：
56.9
作者：
Guler, ML;Gorham, JD;Murphy, KM
通讯作者：
Murphy, KM
影响因子：
15.3
作者：
Szabo, SJ;Dighe, AS;Gubler, U;Murphy, KM
通讯作者：
Murphy, KM
DOI：
10.1164/ajrccm/137.3.716
发表时间：
1988-03-01
期刊：
AMERICAN REVIEW OF RESPIRATORY DISEASE
影响因子：
--
作者：
ORME, IM
通讯作者：
ORME, IM