Biology of Aging
IMMUNE SYSTEM: Can Your Immune System Still Defend You As You Age?
Elementary schools are breeding grounds for the common cold. Kids pass their germs around as often as they share their lunch. For children, catching a cold may not be a big deal. They might take it easy for a few days while their immune system kicks into action and fights off infection. But for their older teachers and grandparents, each cold can be more of a challenge. It may take a week or longer to get back to feeling 100 percent. Does that mean that the immune system gets weaker as we age? That’s what gerontologists are trying to figure out.
Our immune system is a complicated network of cells, tissues, and organs to keep us healthy and fight off disease and infection. The immune system is composed of two major parts: the innate immune system and the adaptive immune system. Both change as people get older. Studies to better understand these changes may lead to ways of supporting the aging immune system.
Innate immunity is our first line of defense. It is made up of barriers and certain cells that keep harmful germs from entering the body. These include our skin, the cough reflex, mucous membranes, and stomach acid. If germs are able to pass these physical barriers, they encounter a second line of innate defense, composed of specialized cells that alert the body of the impending danger. Research has shown that, with age, innate immune cells lose some of their ability to communicate with each other. This makes it difficult for the cells to react adequately to potentially harmful germs called pathogens, including viruses and bacteria.
Inflammation is an important part of our innate immune system. In a young person, bouts of inflammation are vital for fighting off disease. But as people age, they tend to have mild, chronic inflammation, which is associated with an increased risk for heart disease, arthritis, frailty, type 2 diabetes, physical disability, and dementia, among other problems. Researchers have yet to determine whether inflammation leads to disease, disease leads to inflammation, or if both scenarios are true. Interestingly, centenarians and other people who have grown old in relatively good health generally have less inflammation and a more efficient recovery from infection and inflammation when compared to people who are unhealthy or have average health. Understanding the underlying causes of chronic inflammation in older individuals—and why some older people do not have this problem—may help gerontologists find ways to temper its associated diseases.
The adaptive immune system is more complex than the innate immune system and includes the thymus, spleen, tonsils, bone marrow, circulatory system, and lymphatic system. These different parts of the body work together to produce, store, and transport specific types of cells and substances to combat health threats. T cells, a type of white blood cell (called lymphocytes) that fights invading bacteria, viruses, and other foreign cells, are of particular interest to gerontologists.
T cells attack infected or damaged cells directly or produce powerful chemicals that mobilize an army of other immune system substances and cells. Before a T cell gets programmed to recognize a specific harmful germ, it is in a “naïve” state. After a T cell is assigned to fight off a particular infection, it becomes a “memory” cell. Because these cells remember how to resist a specific germ, they help you fight a second round of infection faster and more effectively. Memory T cells remain in your system for many decades.
A healthy young person’s body is like a T cell producing engine, able to fight off infections and building a lifetime storehouse of memory T cells. With age, however, people produce fewer naïve T cells, which makes them less able to combat new health threats. This also makes older people less responsive to vaccines, because vaccines generally require naïve T cells to produce a protective immune response. One exception is the shingles vaccine. Since shingles is the reactivation of the chickenpox virus, this particular vaccine relies on existing memory T cells and has been particularly effective in older people. Researchers are investigating ways to develop other vaccines that are adjusted for the changes that happen in an older person’s immune system.
Negative, age-related changes in our innate and adaptive immune systems are known collectively as immunosenescence. A lifetime of stress on our bodies is thought to contribute to immunosenescence. Radiation, chemical exposure, and exposure to certain diseases can also speed up the deterioration of the immune system. Studying the intricacies of the immune system helps researchers better understand immunosenescence and determine which areas of the immune system are most vulnerable to aging. Ongoing research may shed light on whether or not there is any way to reverse the decline and boost immune protection in older individuals.
Organs of the Immune System
Adapted from www.niaid.nih.gov
The Future of Aging Research: Altering Older Adults’ Immunity
Our ability to survive the germs around us is based on a tightly controlled immune system. Too little of an immune response makes us susceptible to infection, including life-threatening pneumonia. Conversely, an overactive immune response is at the root of autoimmune diseases common among older people and may contribute to age-related chronic diseases like Alzheimer’s disease, osteoarthritis, diabetes, and heart disease. So, should scientists try to change the immune response in older people, or is immunosenescence somehow beneficial within the context of the aging body?
Given the delicate balance of the immune system, gerontologists suspect that, along with its more obvious negative consequences, immunosenescence might have a protective role in seniors. More research is needed before scientists fully understand the aging immune system and determine whether changing an immune response would lead to an increase or a decrease in health span and lifespan in humans.
Publication Date: November 2011
Page Last Updated: March 20, 2014