Plitnick L M, Banas J A, Jelley-Gibbs D M, O'neil J, Christian T, Mudzinski S P, Gosselin E J
Department of Microbiology, Cellular Immunology Laboratory, Albany Medical College, Albany, NY 12208, USA.
Immunology. 1998 Dec;95(4):522-8. doi: 10.1046/j.1365-2567.1998.00631.x.
Generation of an effective cellular immune response is key to the successful development of both humoral and cellular immune defences against most pathogens. However, while the type of cellular immune response elicited by any given pathogen is dictated by the entire array of antigens and molecules which comprise that pathogen, most studies of human immune responses to bacterial pathogens tend to focus on selected antigens. This is a result, in part, of a desire to find those antigens that will generate a desired immune response, as well as limited technology for monitoring the complex array of responses generated by an intact organism. Utilizing Streptococcus mutans as a model Gram-positive organism, a novel flow cytometric assay that permits the identification of individual cells within a responding population, and highly sensitive cytokine assays, we show for the first time that CD8 T cells and natural killer (NK) cells comprise a significant component of the response to this organism in humans. This is despite the fact that CD8 T cells are traditionally thought to respond to endogenously derived antigens only. In addition, we provide the first evidence that a Gram-positive organism can actively inhibit interleukin-2 (IL-2), an important autocrine growth factor for T cells. The latter observation could represent an additional mechanism by which Gram-positive organisms evade host defences.
产生有效的细胞免疫反应是成功发展针对大多数病原体的体液免疫和细胞免疫防御的关键。然而,虽然任何特定病原体引发的细胞免疫反应类型由构成该病原体的所有抗原和分子决定,但大多数关于人类对细菌病原体免疫反应的研究往往集中在选定的抗原上。部分原因是希望找到能产生所需免疫反应的抗原,以及监测完整生物体产生的复杂反应阵列的技术有限。利用变形链球菌作为革兰氏阳性菌的模型,一种新颖的流式细胞术检测方法可识别反应群体中的单个细胞,以及高灵敏度的细胞因子检测方法,我们首次表明,在人类中,CD8 T细胞和自然杀伤(NK)细胞是对该生物体反应的重要组成部分。尽管传统上认为CD8 T细胞仅对内源性抗原作出反应。此外,我们首次提供证据表明,革兰氏阳性菌可主动抑制白细胞介素-2(IL-2),这是T细胞重要的自分泌生长因子。后一观察结果可能代表革兰氏阳性菌逃避宿主防御的另一种机制。