Yunis E J, Lane M A
J Invest Dermatol. 1979 Jul;73(1):24-8. doi: 10.1111/1523-1747.ep12532755.
Our study of the aging process in human beings and in mice is complicated by our need to know whether we are observing diseases of aging or natural nondisease state processes. Results from studies on inbred strains of mice and retrospective studies on HLA types in aging human populations suggest that genetic effects play a significant role in predetermining the life span of an individual. It is clear that in such mouse strains genetic defects that affect cell regulatory mechanisms result in the production of autoimmune reactivity, tumor development, and a shortened life span. In human beings, although results are less clear-cut, strong associations exist between some disease states and the HLA type. Also, the disappearance of HLA-B8 from older women suggests that this HLA type does not confer longevity. Cellular immune reactivity declines with age in all populations studied to date, and cell cooperative or regulatory mechanisms function less well. We need to characterize the specific nature of the cells directly responsible for these alterations and to attempt to correct deficiencies by dietary manipulation or transfer techniques.
我们对人类和小鼠衰老过程的研究因需要确定我们所观察到的是衰老疾病还是自然的非疾病状态过程而变得复杂。对近交系小鼠的研究结果以及对老年人群体中HLA类型的回顾性研究表明，基因效应在预先决定个体寿命方面起着重要作用。很明显，在这类小鼠品系中，影响细胞调节机制的基因缺陷会导致自身免疫反应性的产生、肿瘤的发展以及寿命缩短。在人类中，尽管结果不那么明确，但某些疾病状态与HLA类型之间存在着密切关联。此外，老年女性中HLA - B8的消失表明这种HLA类型并不能带来长寿。在迄今为止研究的所有群体中，细胞免疫反应性都会随着年龄的增长而下降，并且细胞协同或调节机制的功能也会变差。我们需要明确直接导致这些变化的细胞的具体特性，并尝试通过饮食调控或转移技术来纠正缺陷。
