The age-related decline of the immune system is complex. There are many facets to the issues of increased systemic inflammation and reduced immune competence. Here, researchers show that a necessary population of memory B cells is reduced with age, and this impairs the ability of the immune system to respond to novel threats. Clearing the entire B cell complement has been attempted in mice, and shown to improve function. B cells regenerate rapidly following clearance, even in old animals. It is as yet unknown as to how that approach interacts with the dysfunction described here, but B cell clearance does address the problem of an accumulation of dysfunctional age-associated B cells.
Immunological memory is the ability of our immune system to remember previously encountered pathogens. Infections are rare in adults thanks to their large repertoire of specific memory T cells and memory B cells generated by previous antigenic experiences. In the elderly, susceptibility to infections increases again. We focused our attention on B cells that change with age in number and type. As a result of infection or vaccination, B cells become memory B cells (MBCs) and plasmablasts (PBs) able to produce high affinity antigen-specific antibodies. MBCs can be identified by the expression of the CD27 marker. The intensity of expression of CD27 defines two populations, CD27dull and CD27bright MBCs.
We show that the elderly have a significant reduction of CD27dull memory B cells, a population that bridges innate and adaptive immune functions. CD27bright MBCs are generated exclusively by a T cell-dependent mechanism and under a strong selective pressure by an antigen. Compared to children, elderly individuals have more CD27bright MBCs. Taken together, this suggests that their immune system may be equipped to react against well-known antigens but has a reduced ability to respond to new pathogens. Moreover, after in vitro stimulation, B cells from older individuals produced significantly fewer antibodies compared to younger individuals.