The failing immune system of the elderly is characterized by a greatly increased number of memory T cells, and too few naive T cells capable of taking on new threats. One explanation for why this is the case is exposure to cytomegalovirus (CMV), a ubiquitous herpesvirus that the immune system cannot clear. Ever more T cells become uselessly devoted to fighting it until the immune system can no longer do its job. There are research results from human studies to support this view. It isn't the only reason that the immune system fails, but it may be one of the more important ones.
These researchers see a different picture when working in mice, however. To their eyes memory T cells are expanding in number with age due to some other process, something yet to be fully understood. CMV may prove to be a red herring yet, or this may turn out to be a significant difference between the immunology of mice and people:
The number of memory phenotype CD8 T cells increases dramatically with aging in both humans and mice. However, the mechanism for this is unknown. The prevailing hypothesis is that memory T cells accumulate with aging as a result of lifelong antigenic stimulation. However, data supporting this supposition are lacking.
In this study, we demonstrate that central memory CD8 T cells, which represent a large majority of memory CD8 T cells in aged mice, are not memory cells that develop in response to antigenic stimulation but are virtual memory cells that develop without antigenic stimulation. In addition to phenotypic evidence, we show that accumulation of central memory CD8 T cells is independent of CD4 T cells, CCR5, and CXCR3, all of which are known to be essential for [antigen]-driven development of central memory CD8 T cells. Thus, this study reveals a novel mechanism for aging-related changes in CD8 T cells.
The direct short-cut approach here is to destroy all these memory cells, and let the immune system repopulate with fresh new cells, perhaps helping it along with an infusion of cells generated from the patient's own stem cells. It doesn't matter how memory cells come to use up the allotted space for immune cells so long as they can reliably be singled out and cleared away.