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炭疽致死毒素对树突状细胞和适应性免疫的损害。

Impairment of dendritic cells and adaptive immunity by anthrax lethal toxin.

作者信息

Agrawal Anshu, Lingappa Jai, Leppla Stephen H, Agrawal Sudhanshu, Jabbar Abdul, Quinn Conrad, Pulendran Bali

机构信息

Emory Vaccine Research Center, 954 Gatewood Road, Atlanta, Georgia 30329, USA.

出版信息

Nature. 2003 Jul 17;424(6946):329-34. doi: 10.1038/nature01794.

Abstract

Anthrax poses a clear and present danger as an agent of biological terrorism. Infection with Bacillus anthracis, the causative agent of anthrax, if untreated can result in rampant bacteraemia, multisystem dysfunction and death. Anthrax lethal toxin (LT) is a critical virulence factor of B. anthracis, which occurs as a complex of protective antigen and lethal factor. Here we demonstrate that LT severely impairs the function of dendritic cells--which are pivotal to the establishment of immunity against pathogens--and host immune responses by disrupting the mitogen-activated protein (MAP) kinase intracellular signalling network. Dendritic cells exposed to LT and then stimulated with lipopolysaccharide do not upregulate co-stimulatory molecules, secrete greatly diminished amounts of proinflammatory cytokines, and do not effectively stimulate antigen-specific T cells in vivo. Furthermore, injections of LT induce a profound impairment of antigen-specific T- and B-cell immunity. These data suggest a role for LT in suppressing host immunity during B. anthracis infections, and represent an immune evasion strategy, where a microbe targets MAP kinases in dendritic cells to disarm the immune response.

摘要

炭疽作为生物恐怖主义的一种媒介,构成了明显且当前存在的危险。感染炭疽杆菌(炭疽的病原体),若不进行治疗,可能导致猖獗的菌血症、多系统功能障碍及死亡。炭疽致死毒素(LT)是炭疽杆菌的关键毒力因子,它以保护性抗原和致死因子的复合物形式存在。在此我们证明,LT通过破坏丝裂原活化蛋白(MAP)激酶细胞内信号网络,严重损害树突状细胞(对建立针对病原体的免疫至关重要)的功能以及宿主免疫反应。暴露于LT然后用脂多糖刺激的树突状细胞不会上调共刺激分子,分泌的促炎细胞因子量大幅减少,并且在体内不能有效刺激抗原特异性T细胞。此外,注射LT会导致抗原特异性T细胞和B细胞免疫的严重受损。这些数据表明LT在炭疽杆菌感染期间抑制宿主免疫中发挥作用,并且代表了一种免疫逃避策略,即一种微生物靶向树突状细胞中的MAP激酶以解除免疫反应。

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