What is the science for which trio won Nobel for medicine 2025? Explained in simple terms

The alfred bernhard nobel treasure in medical specialty of physiology was proclaimed on oct 6 for three scientists for discovering how a particular kind of cell can stop the body's immune system from attacking itself.

The cells known as “T-cells” are a new hope for fighting autoimmune diseases and cancer.

After Americans Mary Brunkow and Fred Ramsdell and Japan's Shimon Sakaguchi were announced new Nobel laureates at a ceremony in Stockholm, here is what you need to know about their work:

The immune system is your body's first line of defence against invaders such as microbes that could give you an infection. It helps the body protect itself from foreign germs that could harm its health. The most powerful defence of the immune system is white blood cells called T-cells. They seek out, identify and destroy these invading germs or other unwanted outsiders such as cancerous cells throughout the body.

But sometimes these T-cells identify the wrong target and attack healthy cells, which causes a range of autoimmune diseases such as type 1 diabetes and lupus.

Regulatory T-cells, or Tregs, called the body's "security guards" by the Nobel committee, help stop the immune system from attacking healthy cells. "They put the brakes on the immune system to prevent it from attacking something that it shouldn't," said Jonathan Fisher, head of the innate immune engineering lab at University College London.

For a long time, scientists thought this job was done entirely by the thymus, a small gland in the chest. T-cells have special "receptors" that let them recognise harmful invaders, like the spiky Covid-19 virus. While T-cells develop in the thymus, the gland removes any T-cells that could attack the body’s own cells. But what if a few of these harmful T-cells slip through?

Also read: Nobel Prize 2025 winners: Who are Mary Brunkow, Fred Ramsdell and Shimon Sakaguchi?

Earlier, some scientists thought that there could be other cells in the body, and some other cells out there, patrolling for escapees. But by the 1980s, most researchers had abandoned this idea, except Sakaguchi.

His team took the T-cells from one mouse and injected them into another, which had no thymus. The mouse was suddenly protected against autoimmune diseases, showing that something other than the gland must be able to fight off self-attacking T-cells.

About ten years later, Brunkow and Ramsdell were studying why male mice from a mutated strain called "scurfy" only survived for a few weeks. In 2001, they discovered that a mutation in the FOXP3 gene was responsible for both the scurfy condition in mice and a rare autoimmune disease in humans known as IPEX.

Following this, researchers, including Sakaguchi, demonstrated that the FOXP3 gene is essential for the development of regulatory T-cells. Meaning this is the gene which determines the presence of regulatory T-cells.

Also read: Brunkow, Ramsdell and Sakaguchi win 2025 Nobel medicine prize, a look at their prize money

A new field of research has been probing exactly what this discovery means for human health. French immunologist Divi Cornec told AFP that "a defect in regulatory T-cells" can make autoimmune diseases more severe. These cells also play a "crucial role in preventing transplanted organs from being rejected," Cornec said. Cancer can also "hijack" regulatory T-cells to help it escape the immune system, Fisher said.

When this happens, the cells crack down too hard on the immune system, like an overzealous security guard and allow the tumour to grow.

According to the Nobel ceremony, more than 200 clinical trials are currently underway testing treatments that involve regulatory T-cells. However, the discoveries that earned this year’s Nobel Prize have not yet resulted in a widely used drug. On Monday, Sakaguchi expressed hope that the Nobel recognition would help push the field toward real-world clinical applications.

Jonathan Fisher noted that significant progress has been made in the past five years, but reminded that such advances require both time and substantial funding. “There’s still a major gap between what we understand about the immune system in the lab and our ability to turn that into a safe, effective drug that consistently works in humans,” Fisher said.

---

---