Telomeres are segments of DNA that exist on the ends of our chromosomes. With each successive cell division, our chromosomes must be duplicated so that each daughter cell receives a full complement of DNA. With each duplication of the chromosomes, a bit of the telomere is lost, and when the telomeres reach a critically short length, the cells lose the ability to divide. When that critically short length has been reached, the cell is said to enter a phase called replicative senescence, and its functions and activities change. Telomerase is an enzyme that restores the length of telomeres and permits cells to continue dividing. Telomerase is found in many cancerous cells, and is believed to account for the "immortality" of many cancers, i.e., the ability of cancer cells to reproduce indefinitely, without the limits placed on ordinary cells.

The length of the telomeres found in T cells known as CD4+ cells has been found to decrease with increasing age. Telomeres become shorter when naïve T cells, which have never before encountered antigen, are induced to divide and then become mature memory cells. Young T cells have high levels of telomerase activity, while older, mature cells have lower levels of telomerase activity. Interestingly some white blood cells possess the ability to increase their level of telomerase activity, and that ability does not appear to decrease with age. The preservation of telomerase activity means that the shortening of telomeres and the reduction in replicative capacity in at least some lymphocytes or white blood cells is less affected by aging than in others. Further study in this area will further define the various processes that contribute to the decline in immunity as we age, and what, if anything, can be done to reduce its impact.