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白细胞介素-12使CD4 + T细胞在鸟分枝杆菌感染期间产生干扰素-γ并获得保护性免疫。

Interleukin-12 primes CD4+ T cells for interferon-gamma production and protective immunity during Mycobacterium avium infection.

作者信息

Silva R A, Flórido M, Appelberg R

机构信息

Laboratory of Microbiology and Immunology of Infection, Institute for Molecular and Cell Biology, University of Porto, Portugal.

出版信息

Immunology. 2001 Jul;103(3):368-74. doi: 10.1046/j.1365-2567.2001.01237.x.

Abstract

Interleukin-12 (IL-12) is a crucial cytokine for the generation of a protective immune response against Mycobacterium avium infection. In contrast to infected control mice, IL-12-deficient mice were unable to control bacterial proliferation and their spleen T cells were almost unresponsive in vitro to specific antigens of M. avium. Susceptibility of mice deficient in IL-12 was similar to that of interferon-gamma (IFN-gamma)-deficient mice. These data indicate a crucial role of IL-12 in the development of a T-cell population able to produce IFN-gamma and to mediate protection against M. avium infection. Treatment of M. avium-infected mice with IL-12 induced CD4+ T cells with enhanced capacity to produce IFN-gamma as well as to confer increased protection against M. avium.

摘要

白细胞介素-12(IL-12)是针对鸟分枝杆菌感染产生保护性免疫反应的关键细胞因子。与感染对照小鼠相比,IL-12缺陷小鼠无法控制细菌增殖,其脾脏T细胞在体外对鸟分枝杆菌的特异性抗原几乎无反应。IL-12缺陷小鼠的易感性与干扰素-γ(IFN-γ)缺陷小鼠相似。这些数据表明IL-12在能够产生IFN-γ并介导针对鸟分枝杆菌感染的保护作用的T细胞群体的发育中起关键作用。用IL-12治疗鸟分枝杆菌感染的小鼠可诱导CD4 + T细胞产生IFN-γ的能力增强,并增强对鸟分枝杆菌的保护作用。

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