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Longevity

101 Facts About Ageing #48: Autoimmune Diseases And Ageing

Posted on 27 October 2021

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As Daniel Patrick Moynihan, an American sociologist, politician, and diplomat once said: “Everyone is entitled to his own opinion, but not his own facts”. And we wholeheartedly agree. A shared set of facts is the first step to building a better world with longevity for all. In that spirit, we are creating a series that covers 101 indisputable facts about ageing, health and longevity.

Autoimmune disease is a term used to refer to a group of 80 or so diseases in which the immune system mistakenly recognises the body’s own cells as a threat. Autoimmune diseases differ greatly from one another in their effects, depending on which cells are attacked by the immune system. In multiple sclerosis, for example, the immune system attacks the protective coating of the nerve fibres, leading to neurological effects, while in type 1 diabetes, insulin-producing cells in the pancreas are attacked, resulting in insufficient insulin production and elevated blood sugar.

Incidence rates for type 1 diabetes by age at diagnosis and sex, United...  | Download Scientific Diagram
Age at diagnosis of type 1 diabetes.
Source

Older individuals have more autoimmunity (that is to say, they have higher levels of antibodies that target their own cells). However, this often doesn’t translate to a greater risk of diagnosed autoimmune disease. For example, you are most likely to be diagnosed with multiple sclerosis at around age 40, after which the rate of diagnosis greatly declines. Many autoimmune diseases, such as type 1 diabetes, have a heavy genetic component that leads to many cases occurring in childhood or early adulthood (as shown in the graph above). As autoimmune diseases are generally neither curable nor fatal (when treated), the number of people living with autoimmune disease will almost always increase with age, even if diagnosis does not.

Statistic: Share of adults diagnosed with autoimmune conditions in the United Kingdom (UK) in 2018, by age* | Statista
Find more statistics at Statista

With this being said, we know of mechanisms by which ageing may contribute to the development of autoimmunity, although our understanding of what actually triggers autoimmune disease remains poor. Given the decline in number and function of T cells and B cells discussed in fact #49, it may seem counterintuitive that ageing could make autoimmunity more likely. However, ageing doesn’t just decrease the immune system’s offensive ability, but also its ability to weed out those immune cells that might mistake the body’s own cells as the enemy. At the same time, in order to compensate for the reduced production of new T cells, existing T cells start to multiply, which means that any bad apples get amplified and become harder to control.

In fact #29, we covered how ageing is accompanied by increasing levels of circulating inflammatory molecules (inflammageing). Some of these inflammatory signals can help activate T cells, so it is possible that inflammageing makes the activation of autoimmune T cells more likely. Inflammageing is associated with higher levels of damage in tissues throughout the body, which leads to the release of molecules from these tissues. If any T cells are primed to react to one of these molecules, they may be more likely to encounter it due to this increased age-related damage.

Taken together, this means that the immune system is more likely to react to something normally present within the body and begin producing antibodies against it. However, as mentioned earlier, this doesn’t necessarily result in full-blown autoimmune disease. This may be because, even as the likelihood of an autoimmune reaction rises, the strength of that reaction declines due to a weakening immune system.


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    References

    Cytokines in Autoimmunity: Role in Induction, Regulation, and Treatment: https://dx.doi.org/10.1089%2Fjir.2011.0065

    Immune aging and autoimmunity: https://dx.doi.org/10.1007%2Fs00018-012-0970-0

    Age-related autoimmunity: https://dx.doi.org/10.1186%2F1741-7015-11-94

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