Advances in our understanding of the processes of aging have led researchers to significant discoveries about how these mechanisms affect the complex system that serves as the body’s defense force against infection and illness.
The key, it turns out, is the declining ability of the immune system to calibrate its level of inflammatory response. Too much response means too much inflammation, and that causes damage to aging tissue. It’s been termed “inflammaging.”
More than with other organ systems, we’re reminded all the time that our immune systems falter as we get older—every flu season when older people are urged to get vaccinated, and every time the government puts out an alert about a tainted food source. Older people are always more susceptible to everything bad that can attack the human body, even the most routine infections that they easily warded off when they were younger.
Indeed, flu shots put it in high relief: though older people are urged to get them, their effectiveness isn’t very good in those over 65.
Put most basically, aging causes immune cells to become dysfunctional, a condition called immunosenescence that’s like a security gate with a sleeping guard, or none at all. This opens the way to chronic inflammation that increases the likelihood of degenerative diseases such as osteoporosis, atherosclerosis and dementia. It’s also partly because our immune systems become progressively less effective at watching out for tumors that cancer rates increase exponentially with age.
Immunosenescence results from changes in the proportion and function of certain white blood cells, the thymus gland and bone marrow. As we age, there is a decline in the number of white blood cells, called “naïve suppressor T-cells,” that are able to fight off new infections or tumors. These cells are distinguished from other white blood cells by two specific molecules—actually by the presence of one and the absence of the other.
Naïve suppressor T-cells do not have a molecule called CD95 protruding from the membranes of their surfaces. And they do have one called CD28. This is the opposite of other white blood cells and it forms a unique mechanism that allows these cells—called CD95-CD28+ T-cells—to defend against attacks by infectious or cancerous cells.
Here’s how: Cells that do not have CD95 sticking out of them have not yet encountered the foreign substance—the molecular snippet of a specific infection or tumor, called an antigen–that they are uniquely created to recognize. When these cells do encounter that particular antigen, the CD28 molecule on their surfaces enables them to divide rapidly and mount a brisk response to their designated antigen, wiping out the infection or tumor.
As young adults we typically have more than 300 of these cells per microliter of blood—about 40 percent of all our cells at that age. But we lose about 3 percent a year from then on. If you do the math, you can see how compromised the immune system is by the time we reach the age of average life expectancy –and that’s no coincidence. By then our bodies are virtually without the ability to fight off new infections and tumors. It’s why pneumonia and influenza are among the top five causes of death in people 65 and older.
The linear decline in the number of CD95-CD28+ T-cells is so highly correlated with age that it has been called the best biomarker of immune aging discovered to date. What makes it so good is that the presence of these T-cells can be detected at specialized labs from the same blood sample used to do routine complete blood counts (CBC).
As with other biomarkers, periodic monitoring can yield evidence of whether and how much therapies are affecting CD95-CD28+ cell counts.