The immune system also develops wrinkles: what happens when our defenses age?

Aging poses a major economic and health challenge for Western societies. In Spain, for example, one-third of the population will be over 65 by 2055. These figures point to an increase in cases of age-related pathologies , such as cardiovascular disease and cancer, not to mention the rise in the number of people susceptible to infectious and autoimmune diseases.

To prevent or slow these consequences, it's essential to understand the changes our bodies undergo over time. It's easy to understand what happens in our bones, brain, or hormones, but how does aging affect our immune system?

As we will see later, new findings about the nature of autoimmune diseases (when the immune system mistakenly attacks our own body) are providing us with valuable clues in this regard.

Immune system ailments

The immune system can be divided into two branches: the innate and the adaptive. The innate responds quickly to any threat and alerts the adaptive immune system. It involves, among others, two types of white blood cells: monocytes and neutrophils. These cells initiate inflammation, which helps us fight the threats we face. However, inflammatory responses must be short and precise, otherwise the immune system becomes exhausted by maintaining inflammation and its ability to protect us diminishes .

Adaptive immunity takes several days to develop because it acts specifically against the microorganism or cancer cell that threatens us. It is made up of another type of white blood cell: T and B lymphocytes. The former interact with innate immunity, eliminate infected cells, and activate the latter, which produce antibodies. Both generate memory cells that remember the enemies we have faced so that, if they attack us again, we can react more quickly and effectively.

What happens is that, over time, our immune system cells also age in a process called immunosenescence or immunoaging . First, neutrophils and monocytes experience a reduction in their ability to effectively move and eliminate pathogens. And regarding adaptive immunity, the generation of new lymphocytes decreases, making it difficult to confront new pathogens. Although memory cells accumulate, their activation is limited.

This new immune system composition promotes constant inflammation and weaker, more disordered responses to threats. Our aging defenses become clumsy and somewhat slower. All of this contributes to a greater lack of protection against infections, greater damage to our bodies, and, consequently, the development of age-related pathologies .

Autoimmunity: premature aging

But sometimes, the aging of the immune system doesn't correspond to the date of birth. This is what happens to patients with some autoimmune diseases such as arthritis or lupus.

Recently, a new type of B lymphocyte has been discovered—the so-called age-associated B cells, or ABC cells —whose numbers naturally increase with age. However, their abundance can increase in other situations.

Although it was initially thought that their function was solely to produce antibodies against pathogens, it has been proven that they also play a central role in autoimmunity. That is, these cells produce antibodies against parts of our own bodies and activate other lymphocytes, which contributes to sustained inflammation .

In this situation, inflammation aggravates the disease, affecting various tissues, including blood vessels. And this is where we find a connection between autoimmune diseases and certain ailments common in old age.

Cardiovascular diseases: enemy number one

Cardiovascular disease is the leading cause of death worldwide , and age is one of the main risk factors. Furthermore, many patients with autoimmune diseases are more likely to develop heart disease than healthy individuals of the same age and sex .

A key event that precedes many cardiovascular diseases is the formation of cholesterol plaques. This process is fueled by inflammation, which damages blood vessel cells, promotes cholesterol deposits, and prevents their removal by macrophages, thereby increasing the size of the plaques . Thus, changes that alter the functioning of our immune systems can promote the growth of cholesterol plaques and, consequently, the risk of cardiovascular disease.

Since all these changes accumulate, it's easy to understand that the risk will increase with age, although this is not always the case. Sometimes, our immune system ages prematurely, which explains why age-related illnesses appear in young people, much earlier than expected. In fact, ABC cells have been shown to play a role in cardiovascular disease that cannot be explained by an individual's date of birth . In this case, the age of the immune system is more important than the age shown on the ID.

These kinds of discoveries could open new horizons for slowing the aging of the immune system, improving the quality of life of the elderly, and helping to find solutions to various pathologies. The relationship between autoimmune diseases and cardiovascular disease could be a key to increasing our longevity. Perhaps the immune system holds the fountain of eternal youth.

Daniel Miranda Prieto is a predoctoral researcher in Immunology at the University of Oviedo .

Javier Rodríguez-Carrio is a professor of Immunology at the University of Oviedo .

This article was originally published on The Conversation .