Rheumatoid arthritis is characteristically a disease of young women, as I was once told by an old man in the medical profession. That is a little of an exaggeration, but autoimmune diseases are not age-related by and large. Can they teach us anything about aging, however?
With this question in mind, you might think of accelerated aging conditions such as progeria, conditions that are not in fact accelerated aging, despite appearances, but rather a single form of damage run amok due to genetic mutation. In the case of progeria, this damage involves malformed lamin proteins, something that does seem to occur in a very minor way in normal aging. Researchers are still digging in to what might be learned there - it remains elusive as to whether this is in any way important, or a cause or a consequence, in normal aging.
Another example is the study of type 2 diabetes. This is a condition often used as a proxy for aging in animal studies, as the effect on some measures of health is to speed up the normal decline. But that doesn't mean it is accelerated aging any more than is progeria. Aging is cellular and molecular damage and the consequences of that damage. There are lots of ways to induce damage in an organism, but that doesn't mean that the type of damage you are looking at has any great relevance to aging. Some do, some don't, and some have only a very narrow relevance in some cases. It all depends on the details.
Back to rheumatoid arthritis, as there are researchers who argue that some of its effects can be categorized as an accelerated aging of the immune system. A fair fraction of the frailty of age stems from vulnerability to infections and a growing inability of the immune system to clear out senescent and potentially cancerous cells. As long-term readers will know by now, the immune system malfunctions with age for reasons that are at least partially structural, falling into a state of chronic inflammation coupled with increasing ineffectiveness. The question for today is whether the forms of damage and malfunction exhibited in rheumatoid arthritis are at all relevant to the normal progression of immune aging: the result looks like accelerated aging at the high level, in terms of reduced function and changes in various measures, but is there actually any overlap in the type of causative damage involved?
Some opinions on the subject follow in an open access paper, but it's worth remembering that rheumatoid arthritis might be one of the least understood of the common autoimmune conditions. Despite a great deal of work, researchers haven't yet resolved its causes or more than a fraction of the mechanisms involved in driving the condition. It may even be several quite distinct conditions lumped under this one heading, all with a similar outcome but deriving from different origins. It's a complex field, one with plenty of room for debate in the absence of a full picture that joins all of the puzzle pieces together.
Many of the aging-related morbidities, including cancer, cardiovascular disease, neurodegenerative disease, and infectious susceptibility, are linked to a decline in immune competence with a concomitant rise in proinflammatory immunity, placing the process of immune aging at the center of aging biology. Immune aging affects individuals older than 50 years and is accelerated in patients with the autoimmune disease rheumatoid arthritis.
Immune aging results in a marked decline in protective immune responses and a parallel increase in tissue inflammatory responses. By studying immune cells in patients with rheumatoid arthritis, several of the molecular underpinnings of the immune aging process have been delineated, such as the loss of telomeres and inefficiencies in the repair of damaged DNA. Aging T cells display a series of abnormalities, including the unopposed up-regulation of cytoplasmic phosphatases and the loss of glycolytic competence, that alter their response to stimulating signals and undermine their longevity.
Understanding the connection between accelerated immune aging and autoimmunity remains an area of active research. With increasing knowledge of the molecular pathways that cause immunosenescence, therapeutic interventions can be designed to slow or halt the seemingly inevitable deterioration of protective immunity with aging.
Research into the effects of HIV infection and AIDS on the immune system is another area with a similar relationship to normal immune aging, I should mention. There are those who think that at least some shared mechanisms are at work in both cases.