Pawelec G, Koch S, Franceschi C, Wikby A
University of Tübingen Medical School, Center for Medical Research, ZMF, Germany.
Ann N Y Acad Sci. 2006 May;1067:56-65. doi: 10.1196/annals.1354.009.
The rate of acceleration of the frequency of death due to cardiovascular disease or cancer increases with age from middle age up to around 75-80 years, plateauing thereafter. Mortality due to infectious disease, however, does not plateau, but continues to accelerate indefinitely. The elderly are particularly susceptible to novel infectious agents such as SARS, as well as to previously encountered pathogens. Why is this? The elderly commonly possess oligoclonal expansions of T cells, especially of CD8 cells, which, surprisingly, are associated with cytomegalovirus (CMV) seropositivity. This in turn is associated with many of the same phenotypic and functional alterations to T cell immunity that have been suggested as biomarkers of immune system aging. We suggest that, in fact, CMV, not age per se, is the prime driving force behind many or most of the oligoclonal expansions and altered phenotypes and functions of CD8 cells in the elderly. Thus, the manner in which CMV and the host immune system interact (over which period? on which genetic background? with which co-infections?) is critical in determining the "age" of adaptive immunity and hence human longevity. In this respect, immunosenescence is infectious.
心血管疾病或癌症导致的死亡率加速率从中年到75 - 80岁左右随年龄增长而增加，此后趋于平稳。然而，传染病导致的死亡率并未趋于平稳，而是持续无限加速。老年人尤其易受新型传染因子如非典的影响，也易受先前接触过的病原体影响。这是为什么呢？老年人通常拥有T细胞的寡克隆扩增，尤其是CD8细胞，令人惊讶的是，这与巨细胞病毒（CMV）血清阳性有关。这反过来又与许多相同的T细胞免疫表型和功能改变有关，这些改变被认为是免疫系统衰老的生物标志物。我们认为，事实上，CMV而非年龄本身是老年人许多或大多数CD8细胞寡克隆扩增以及表型和功能改变背后的主要驱动力。因此，CMV与宿主免疫系统相互作用的方式（在哪个时期？在何种遗传背景下？伴有哪些合并感染？）对于确定适应性免疫的“年龄”进而人类寿命至关重要。在这方面，免疫衰老具有传染性。
