The aging of the adaptive immune system, made up of B cells and T cells, is a complex process. Broadly, the pace at which new adaptive immune cells are created declines to a tiny fraction of youthful levels in most people by age 50, and this lack of replacements allows the adaptive immune system to become ever more populated by exhausted, senescent, and malfunctioning cells. This decline in the supply of new adaptive immune cells is in part a problem of hematopoietic cells in the bone marrow, responsible for creating B cells and thymocytes that migrate to the thymus to mature into T cells. The decline is also in part a problem of the thymus, which atrophies with age, and of the lymphoid organs such as lymph nodes where B cells mature, which suffer their own age-related declines in structure and function.
Beyond the problems that arise from impaired replenishment of the adaptive immune system populations, it is also the case that immune cells, like all other cells, exist in the aged tissue environment, and will react in some combination of adaptive and maladaptive ways to the presence of damage, altered signaling, increased inflammation, and so forth. Today's open access paper presents data on what looks to be a consequence of this second class of issues, an altered secretion of signals by a subpopulation of T cells throughout the aged body that contributes to loss of cognitive function via disruption of normal operations in the hippocampus.
