The autoimmune theory of aging, introduced by Roy L. Walford in 1969, asserts that with age, the immune system tends to lose efficiency and experiences widespread dysfunction, evidenced by autoimmunity (immune reactions against one's own body proteins) and a decreased ability to respond to infection and other immune challenges. Human immunity is a highly regulated and coordinated process, and is often divided into two components. The first, known as innate immunity, provides a defense against pathogens (potential disease‐causing agents) in a nonspecific way; and the second, known as adaptive or protective immunity, involves a specific response to a pathogen that the body has seen before. Once the body is exposed to an antigen (a foreign substance or pathogen capable of causing an immune response), antibodies will be produced that specifically target that antigen.

There are many different types of cells that are involved in protecting the body against infection; the primary cells involved in the adaptive immune response are called B and T cells. B cells, which function to produce antibodies, are produced in the bone marrow. The bone marrow is the tissue located in the inside of larger bones, where red blood cells, white blood cells (immune cells), and platelets are produced. Immature white blood cells mature into T cells in the thymus gland, which lies in the upper part of the chest. There are several types of T cells, including helper T cells that produce chemical signals in order to initiate the immune response, and cytotoxic T cells responsible for destruction of antigen‐bearing targets.

Age‐Related Changes to the Immune System

As a person ages, the thymus gland progressively shrinks in size and decreases functionality. While the absolute number of cells remains relatively constant, T‐cell function and responses are decreased, making the elderly more susceptible to the development of tumors and decreasing a person's ability to fight against viral illnesses. The amount and type of antibodies produced in response to immune stimuli are also decreased with age. This may be due to an increased proportion of senescent (nondividing) cells with age (see Cellular theory of aging) or a general degeneration of the cells of the immune system. The lack of this antibody response makes the elderly more susceptible to infectious diseases.

As a person ages there are several notable changes to the immune system, one of which is an increase in autoantibodies. These are antibodies that have lost their ability to distinguish “self,” cells of the individual aging person's body, from “nonself.” Examples of “nonself” cells are cells that are infected with a pathogen, cancer cells, pathogenic organisms, or foreign cell types that have infiltrated the body. Instead of having specificity for “nonself” antigens, these antibodies attack “self” antigens, leading to the dysfunction and destruction of normal body tissues—a phenomenon often referred to as autoimmune disease. The development of autoantibodies may potentially result from genetic errors that accumulate with age in cells of the immune system (see Error accumulation theory of aging).

Despite the observed increase in the number of these autoantibodies, the incidence of autoimmune diseases has not been shown to increase with age. Some examples of automimmune diseases are systemic lupus erythematosus, a systemic autoimmune disease affecting many parts of the body including the skin, kidneys, lungs, joints, blood vessels, and brain, and myasthenia gravis, a rare muscular disease associated with progressive weakness of the eyes, face, and neck muscles, in which autoantibodies attack neuromuscular junctions (areas where the nerves that control muscle function and muscle fibers meet). Other more commonly recognized autoimmune diseases include rheumatoid arthritis, insulin‐dependent diabetes mellitus, and multiple sclerosis.

Public Health Perspective

Health‐care professionals, public health professionals, and personal caregivers responsible for the care of aging adults must be aware and account for the changes in the immune system with age. There is also significant interindividual variability in the immune response, with many elderly individuals having normal immune function. Recognizing this variation may be particularly important for those involved in clinical research with the elderly, since this variability may limit the generalizability of study results. Although studies have not drawn a causal link between immune dysfunction and an increased incidence of autoimmune diseases or increased rates of specific infections, the elderly have been shown to experience disproportionate morbidity and mortality related to these conditions and to decreased immune functioning. Elderly people should therefore be closely monitored for the development of age‐associated autoimmune diseases or cancers, and should be treated promptly and aggressively.

Given the potential for reduced defenses against infections, elderly adults should be vaccinated to prevent infections from occurring and should be given additional care as required, when faced with common infections. These precautionary measures are particularly important because the elderly tend to experience more comorbid disease and use more medications. Both comorbidity and medication usage can lead to compromised immune function and limit the ability to cope with infection and disease. Supplementation with immune‐stimulating nutrients and vitamins or medications to encourage immune‐cell regeneration may prove helpful in preventing some of the negative effects of age‐related immune system dysfunction.

Related Topics

Arthritis, Cellular theory of aging, The error catastrophe (accumulation) theory of aging, Immunizations, Multiple sclerosis, Polypharmacy, Vitamins