Given that autoimmune diseases are the third most widespread category of human illnesses (after cancer and cardiovascular diseases), this year’s Nobel Prize in Medicine not only makes sense but also confirms the reality of our times. It is estimated that about 10% of the global population suffers from some autoimmune disorder. The 2025 Nobel Prize in Medicine was awarded to three scientists who managed to decode the mechanism behind the origin of such diseases.

Simply put — since “autoimmune” is often a euphemism for “incurable” and “unexplained” — the 2025 Nobel Prize in Medicine marks a decisive step toward addressing more than 150 autoimmune disorders that affect, and sometimes threaten, the lives of over 800 million people worldwide. The groundbreaking research that earned the Nobel — conducted by one Japanese and two American scientists — is also linked to potential developments in cancer treatments, in preventing organ transplant rejection, and more.

A Rapid Increase

As for autoimmune diseases themselves, not only have they been steadily increasing over the past 20–30 years — in both the number of patients and the range of diseases — but they also remain, to a large extent, a “black hole” for science. After all, it is fundamentally perplexing why the human body would try to harm itself — to self-torment or even self-destruct.

And yet it does so using its most effective means of survival: the immune system. Autoimmune diseases are precisely the result of a mysterious tendency of the body to trigger a self-destructive pathological condition, such as multiple sclerosis, lupus, myocarditis, type 1 diabetes, psoriasis, rheumatoid arthritis, and many others.

The immune system, at its core, is a complex biological war machine — the most powerful shield the human body possesses against disease-causing enemies. In simple terms, its mission is to repel and neutralize viruses and pathogens from the environment, preventing the creation of dysfunctional or harmful cells. After millions of years of evolution and adaptation to ever-changing conditions, the immune system is considered one of evolution’s greatest miracles — a stunning masterpiece of natural biotechnology.

The Nobel Laureates

The recipients of this year’s Nobel Prize in Medicine — Japanese immunologist Shimon Sakaguchi, professor at Osaka University; American researcher Mary E. Brunkow of Princeton; and Fred Ramsdell of Sonoma Biotherapeutics in San Francisco — after years of research, managed to understand how the immune system can be regulated to prevent unwanted deviations and derailments. In other words, they uncovered what happens when the immune system becomes confused and attacks the human body instead of defending it against external threats — countless microbes, bacteria, and viruses, such as COVID-19.

Deceptive Cells

Many of the body’s unseen enemies are so cunning that they “disguise” themselves to resemble healthy cells. Normally, however, the immune system is not easily deceived; it has the remarkable ability to distinguish harmful invaders even when camouflaged. Yet the question arises: why does this highly sophisticated system sometimes “go mad” and suddenly lose its ability to tell healthy cells from harmful ones? And how often does this happen? Why does the immune system rebel in only one out of every ten people? Moreover, can COVID-19 infection — or even vaccination against it — trigger autoimmune disease?

The answers to most of these questions remain vague at best. The 2025 Nobel Prize in Medicine is clear evidence that science is making progress in understanding autoimmunity, but the road to treatment or prevention is still long. The three laureates focused on the root of autoimmunity and its fundamental mechanisms, while other researchers are investigating, for example, possible links between COVID-19 and autoimmune onset.

The “Molecular Mimicry” Phenomenon

Recently, a study revealed the paradoxical phenomenon known as molecular mimicry. In simple terms, certain viruses — such as the coronavirus that caused the global pandemic at the end of 2019 — possess molecules that imitate the body’s own proteins. This confuses the immune system, which, in mobilizing to fight the virus, ends up attacking its own cells. This process is associated with autoimmune diseases such as type 1 diabetes, ankylosing spondylitis, multiple sclerosis, and others.

Stress and Lifestyle Factors

“Autoimmune diseases are not just increasing — they’re skyrocketing,” says Dr. Eleni Komninou, rheumatologist and director of the Clinic for Autoimmune Rheumatic Diseases at Metropolitan General Hospital, speaking to Proto Thema. Although detailed statistics for Greece are lacking, her daily clinical experience confirms the global estimate that around 10% of the population is affected by autoimmune disorders.

According to Dr. Komninou, “We observe an upward trend every year across all, or at least the most common, autoimmune diseases. This increase isn’t only due to better diagnosis or greater public awareness. Cases are multiplying in absolute numbers. And we now believe that heredity doesn’t play the main role. Instead, the triggers are largely related to lifestyle — stress, poor diet, substance abuse — and environmental conditions, such as air pollution. It’s also true that autoimmunity can be associated with pregnancy; it may appear during or after gestation, often combined with a genetic predisposition.”

A Troubling Global Trend

The global rate of increase in autoimmune diseases is alarming — around 19.1% per year. Specifically, Systemic Lupus Erythematosus (SLE) and Sjögren’s Syndrome — a disorder affecting the tear and salivary glands — are increasing by 7.1% annually, according to data from the Sjögren Institute, an international organization monitoring these diseases.

80% of Patients Are Women

For women in particular, the statistics are striking: 80% of autoimmune patients are female. This is linked to genetic factors, as the X chromosome is considered a strong catalyst in autoimmunity. Each human cell contains 23 pairs of chromosomes. In 22 of these pairs, the chromosomes are identical (either XX or YY), but the 23rd pair determines sex — males have XY, females XX.

Studies of individuals with an extra X chromosome — such as men with Klinefelter syndrome (XXY) or women with Triple X syndrome (XXX) — show that autoimmune diseases are 2.3 to 6.6 times more frequent, pointing to the X chromosome as a key suspect in autoimmune susceptibility.

Almost Since the Beginning

For decades, modern scientists believed that immune cells matured according to a protocol known as Central Immune Tolerance. However, as early as the 1980s, Shimon Sakaguchi argued that the scientific community should not place its hopes in Central Tolerance, but rather in Peripheral Immune Tolerance.

Sakaguchi persisted in his experiments using guinea pigs, from which he removed the thymus gland — an organ of pivotal importance to the immune system, functioning much like the control unit of a computer. After countless experiments and studies, Sakaguchi succeeded in decoding the function of Regulatory T cells (T-regs), particularly in understanding how these cellular bodyguards prevent other immune cells from deviating and causing autoimmune diseases.

Moreover, it is the T-regs that moderate the intensity of the body’s defensive response once the alarm has ended — that is, after the invading pathogen (such as a viral infection) has been successfully repelled.

Science Fiction Turned Reality

Following the discoveries of Sakaguchi, Brunkow, and Ramsdell, as well as those of other scientists devoted to the study of autoimmunity, current research focuses on the artificial multiplication of Regulatory T cells. In pilot experiments, the substance interleukin-2 is administered, which has been observed to act like an anabolic agent for T-regs, dramatically boosting their proliferation. One of the key scientific questions is whether interleukin-2 could not only help prevent autoimmune manifestations but also promote the acceptance of transplanted organs by the body.

Another truly fascinating direction of research involves the direct manipulation of T-reg behavior by biologists. The entire endeavor strongly evokes science fiction — yet it is scientific reality. Specialists attach antibodies to the surface of T-regs, which function like identity tags and geographical coordinates.

By adding these antibodies to the cellular structure of the Regulatory T cells, scientists attempt to send them like a protective guard to specific organs — for example, to a transplanted kidney — in order to protect it and prevent rejection, in cases where the body instinctively perceives the graft as a foreign and harmful entity. After all, that instinctive rejection is, by definition, the very purpose of the immune system.