Infectious diseases are a significant cause of death among older adults. Many believe that the decline in immune function that occurs with age is largely responsible. Researchers have found that innate immunity-the immune reaction we mount to any invading germ or foreign substance (as distinct from acquired immunity, directed at specific invaders)-remains relatively intact as we age. Although results vary, many studies confirm that natural killer T cell activity is preserved even among the oldest old. Indeed, some studies have suggested that a decline in natural killer cell activity predicts an increasing risk of serious illness. However, there are some age-related declines in T cell function that affect B cell function, specifically the ability of B cells to help T cells fight infection.

Much research is being done in various laboratories to determine just what changes take place in the various sub-populations of T cells as we age. Researchers at the University of Michigan, led by Richard A. Miller, Ph.D., have utilized mouse T cells as models of what happens in the aging immune system. They have looked at the biochemical changes in T cells that are triggered by an encounter with a foreign molecule, changes that prepare the T cell to help fight off the invader. In an article published in 1999, these scientists demonstrated that one of the proteins in the T cell, called protein kinase C-theta, reacts to the presence of foreign antigens by moving to the area of the T cell that is touching the nearby antigen-presenting cell. The number of T cells that could move the protein kinase to the correct area declined in older mice to about half the number that could respond appropriately in young mice, thus reducing the effectiveness of the aged T cells to react properly to foreign substances.

In work published in 2000 in the Journal of Immunology, these University of Michigan researchers looked at other proteins and molecules contained within T cells crucial to proper immune responses. Two of these proteins are called LAT and Vav. They demonstrated that the ability of T cells to mobilize these proteins to the surface, where they can properly interact with the antigen-presenting cells, also declines about two-fold in aged mice. At the same time, the mice T cells also experience a two-fold decline in their ability to relocate certain proteins to the nucleus, where these proteins normally set off events leading to T cell division and the formation of clones of protective T cells.

It is hoped that this increasingly precise understanding of the aging immune system can one day tested and confirmed in humans, holding out the hope, ultimately, of developing interventions that can boost or at least maintain our immune response over time.