Autoimmunity refers to the unfortunate phenomenon in which our bodies start attacking our own organs and cells as if they were foreign materials. Research suggests that autoimmunity increases as we age, though the incidence of new autoimmune diseases peaks in middle age.

Autoimmune diseases
There are a great many autoimmune diseases that can occur when the human immune system turns on itself. Some of these include rheumatoid arthritis, lupus, autoimmune thyroiditis, polymyalgia rheumatica, giant cell arteritis, and a host of others with long, often difficult-to-pronounce names.

Some of the autoimmune diseases seen more commonly among older adults include polymyalgia rheumatica, which produces joint and muscle pains, and temporal arteritis, an inflammatory problem that damages the arteries near the temples. While rheumatoid arthritis can occur in young adults, there is a recognized, late-onset rheumatoid arthritis as well.

Some background
Antibodies are proteins our immune system makes to attack foreign substances, such as bacteria and viruses. Autoantibodies are immune proteins that we mistakenly make against some part of ourselves. We can sometimes erroneously make antibodies to our own DNA (anti-nuclear antibodies or ANA); to our own mitochondria, the powerhouses of our cells (AMA); and to parietal cells in our stomachs (PCA), among other tissues. When these autoantibodies are organ specific, they attack our organs and cause disease. When they are not organ-specific, they appear to circulate harmlessly in our blood.

Not sure about this?
In a small study that compared younger subjects (under age 60) to older adults (up to age 93) and centenarians (6 men and 20 women, ages 101-106), scientists in Palermo, Italy, found that organ-specific antibodies, the ones that can cause clinically significant disease, are found at the highest rate among the older adults. Centenarians had about the same number of organ-specific autoantibodies as the younger subjects. Non-organ-specific autoantibodies, however, were found at relatively high levels among the centenarians. The study suggests a provocative theory: that those older adults with organ-specific antibodies are less likely to survive to become centenarians. The authors also speculate that the non-organ specific autoantibodies the centenarians have were not made to erroneously attack native tissue, but perhaps were made in response to damage in those tissues as a result of aging. More research, of course, is needed to further clarify these ideas.