The immune system is often imagined as a tireless army defending the body from infections. But it, too, changes with age—and in some cases, the very battles it fights can weaken its future defences. From the burden of memory T cells to the slow formation of artery-clogging plaques, immunological ageing helps explain why heart disease, stroke, cancer and dementia become more common as we grow older.
Why the body makes fewer new immune cells
Producing new T cells is energetically expensive. From an evolutionary point of view, it often made more sense for the body to direct energy towards reproduction in early adulthood rather than maintaining immune strength into old age.
For most of human history, people lived in small groups and rarely travelled beyond the range of their clan. By around the age of 20, a person had likely encountered most of the germs they would ever face. The body could therefore conserve energy by producing fewer new immune cells and relying on memory T cells—cells that remember past infections—to handle familiar threats.
This is an example of antagonistic pleiotropy and disposable soma theory: traits that conserve resources for reproduction early in life can impose costs later. In today’s world, where people live for decades longer and are constantly exposed to new infections, that trade-off becomes more costly.
When memory becomes a burden
Memory T cells can survive for decades. When an old infection returns, they can multiply rapidly: a small number of cells can expand into millions, forming what is effectively a clone army.
But this rapid division comes at a price. Repeated cell division can cause DNA damage and shorten telomeres, leading to cellular damage and senescence in immune cells. Over time, this weakens the immune system’s ability to respond effectively.
Infections themselves can also age the immune system. Persistent pathogens can make it overly focused on old enemies, reducing its capacity to deal with new threats. The most significant example is cytomegalovirus (CMV), a relative of genital herpes and chickenpox. Most people catch CMV at some point in life, and once infected, they never fully clear it.
As people age, T cells specialised for fighting CMV can occupy up to a third of the body’s “immune memory.” This leaves less room for the immune system to learn how to respond to new infections.
The immune system and cancer
The immune system does more than fight external threats. It also monitors the body from within, seeking out and destroying senescent cells—damaged cells that have stopped dividing but can drive inflammation.
It also watches for cancer. Immune cells try to detect cells that are accumulating the genetic changes needed to become tumours but have escaped senescence or apoptosis, the process of programmed cell death.
Cancer becomes more common with age partly because immune function declines. As the immune system weakens, early tumours have more time to grow unchecked.
How immune cells help build artery plaques
Heart disease may seem far removed from immunology, but the immune system plays a central role in atherosclerosis—the process behind many heart attacks and strokes.
Arterial plaques are not simply deposits of cholesterol. They are, in effect, graveyards of immune cells that died after becoming overloaded with cholesterol.
Cholesterol is essential for the body. It helps build cell membranes, the structures that hold a cell’s contents together. The problem arises when cholesterol becomes trapped in the walls of arteries.
A plaque often begins with a small injury to the artery wall. Immune cells in the blood rush to the site to clear the damage and make space for repair. Often, the material they encounter is cholesterol.
Macrophages—literally “big eaters”—are immune cells that engulf harmful material. At first, they clear cholesterol effectively. But when there is too much cholesterol, or when it has been altered by reactions with oxygen and sugars, macrophages struggle to process it.
Instead of discarding the cholesterol, they begin storing it in fatty globs called lipid droplets. These overloaded cells look foamy under a microscope and are known as foam cells. This is the first stage of atherosclerosis.
Eventually, the burden overwhelms the macrophages, and they die. More macrophages then arrive to clear the debris—but the debris contains the same damaged cholesterol that killed the previous cells. The cycle repeats, creating an ever-larger pool of dead cells and damaged cholesterol.
From fatty streaks to heart attacks
Over time, this accumulation becomes visible inside the artery as a fatty streak. These can begin forming in childhood or adolescence, but it usually takes decades before they develop into dangerous plaques.
A mature plaque is a complex structure: a core of dead macrophages and cholesterol, held in place by other cells that attempt to contain it. The plaque creates a bulge in the artery wall, narrowing the vessel and reducing blood flow.
This becomes dangerous when blood flow is severely restricted. A blockage in an artery supplying the heart can reduce oxygen supply, causing chest pain and shortness of breath. Narrowed arteries supplying the penis can also cause erectile dysfunction by disrupting the blood flow needed for an erection.
The most dangerous situation is plaque rupture. When a plaque breaks open, its semi-solid contents spill into the bloodstream and can block smaller vessels. If this happens in an artery supplying the heart, it causes a heart attack—a complete loss of oxygen to part of the heart muscle.
Symptoms can include chest pain, shortness of breath and an overwhelming sense of dread. Immediate hospital treatment is essential; if the blockage is cleared quickly, some heart muscle may be saved. Even then, the heart is likely to be left weaker, and because heart muscle cells turn over very slowly, full recovery is unlikely.
Stroke and vascular dementia
A plaque fragment can also travel to the brain. A blocked vessel there causes an ischaemic stroke—a stroke caused by loss of oxygen to part of the brain.
If a larger vessel is blocked, the effects can be immediate: weakness in the face or arm, loss of speech, blurred vision or dizziness. Anyone experiencing these signs needs urgent hospital care.
Smaller blockages may cause minor or unnoticed damage. But over years or decades, repeated mini-strokes can accumulate, reducing memory and brainpower. This condition is known as vascular dementia, the second most common form of dementia after Alzheimer’s, accounting for about 20 per cent of cases.
Stroke is a major cause of death worldwide, responsible for around 10 per cent of deaths globally. Even when it is not fatal, it can leave people with lasting difficulties in movement, speech, understanding or vision.
A quiet process with deadly consequences
The immune system’s inability to clear damaged cholesterol from artery walls has enormous consequences. Depending on the region, heart attacks and strokes caused by atherosclerotic plaques are responsible for roughly one in five deaths.
It is a striking thought: a microscopic drama involving immune cells, cholesterol and dying macrophages inside artery walls may compete with cancer as one of the deadliest processes in human biology.
Source : Ageless: The New Science of Getting Older Without Getting Old by Andrew Steele
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