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首页> 外文期刊>Experimental Gerontology >Impaired natural killer cell function as a consequence of aging.
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Impaired natural killer cell function as a consequence of aging.

机译：衰老导致自然杀伤细胞功能受损。

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摘要

Alex Comfort wrote (1979): "... nobody needs long-lived mice." His point was, of course, that as much as possible, research should be done with humans "... who are the beneficiaries in mind ..." In this paper we hope to show that long-lived mice have been useful, if not essential, for conducting studies on the aging of innate immunity, specifically the NK cell component of the system. NK cells are activated early in the course of Trypanosoma musculi infections, which we employ as a model. We have generated evidence that the relatively severe infections of aged mice with T. musculi, are attributable, in part, to (a) functionally defective NK cells, the defect(s) being retained by LAK cells that arise from them, and (b) deficient amounts of IL-2 required to convert NK to LAK cells. Defective macrophages, which are the effector cells responsible for eliminating T. musculi, may also accumulate in aged animals. We postulate that the functionally deficient NK cells fail to generate adequate amounts of IFN gamma (and perhaps, TNF alpha) to optimally activate macrophages. This inadequacy can explain the weak ability of aged mice to control the early stage of T. musculi infection preceding the appearance of the more slowly-developing acquired immune response.
机译：亚历克斯·康福特（Alex Comfort）（1979）说：“……没人需要长寿的老鼠。”当然，他的观点是，应该对人类“……谁是受益者……”进行尽可能多的研究。在本文中，我们希望证明，如果对于进行先天免疫（特别是系统中的NK细胞组件）衰老的研究不是必需的。在我们作为模型的锥虫锥虫感染过程中，NK细胞被早期激活。我们已经产生了证据，表明衰老小鼠被T. musculi感染相对较严重，部分原因可归因于（a）功能缺陷的NK细胞，该缺陷由它们引起的LAK细胞保留，和（b ）将NK转化为LAK细胞所需的IL-2量不足。有缺陷的巨噬细胞是负责消除小家蝇的效应细胞，也可能在衰老的动物中积累。我们假设功能缺陷的NK细胞无法产生足够量的IFNγ（也许是TNFα）来最佳地激活巨噬细胞。这种不足可以解释衰老小鼠在出现较缓慢发展的获得性免疫应答之前控制薄壁线虫感染早期的能力较弱。

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