Explainer: The quiet revolution in immunology that earned this year's Nobel Prize
By revealing how the immune system is kept in check, the laureates have not only solved a fundamental biological riddle but also opened practical routes to treat diseases that affect millions worldwide
The 2025 Nobel Prize in Physiology or Medicine has been awarded jointly to Mary E Brunkow, Fred Ramsdell and Shimon Sakaguchi for their discoveries concerning peripheral immune tolerance, an advance the Nobel Assembly said has revolutionised understanding of how the immune system is prevented from attacking the body's own tissues.
The initial breakthrough — regulatory T cells
Shimon Sakaguchi's experiments in the mid-1990s identified a specialised population of T cells, now called regulatory T cells or Tregs, which function as critical suppressors of excessive immune responses; removing or disabling these cells in animal models produced widespread autoimmunity, proving that immune tolerance is not achieved only in the thymus but also in the body's periphery.
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The genetic link — FOXP3
In 2001 Mary Brunkow and Fred Ramsdell pinpointed a mutation in a gene they named Foxp3 in a mouse strain known as scurfy, and showed that equivalent mutations in humans cause the severe immune disorder IPEX; this established FOXP3 as a master regulator necessary for Treg development and function, thereby linking cell biology to genetic mechanisms of immune control.
How these findings reshaped immunology
Taken together, the discoveries solved a longstanding puzzle in immunology — why the body usually tolerates its own tissues despite the presence of self‑reactive immune cells — and launched the field of peripheral tolerance, which now underpins much contemporary research into autoimmunity, transplantation biology and cancer immunology.
Clinical implications and therapeutic directions
The conceptual clarity provided by identifying Tregs and FOXP3 has led to diverse therapeutic strategies: researchers are developing ways to boost Treg activity to treat autoimmune conditions such as type 1 diabetes and multiple sclerosis, and conversely to inhibit or reprogram Tregs to enhance anti‑tumour immunity in cancer patients; early‑phase clinical trials and cell‑therapy approaches are already under way, though researchers caution that translating complex immunoregulatory biology into safe, reproducible treatments remains challenging.
Experts on timelines and challenges
Clinical experts interviewed in the wake of the prize emphasise cautious optimism: while the basic science is mature enough to support translational efforts, timelines to routine clinical application will vary by disease area, with some immune‑suppression strategies possibly taking several years to demonstrate consistent efficacy and safety in large trials, and other approaches — notably cell‑based Treg therapies — expected to require careful scaling and regulatory scrutiny before widespread use.
Why sustained funding and global collaboration matter
The award also underscores the importance of long‑term investment in basic research and international collaboration: breakthroughs such as these emerged over decades from many laboratories, and continued public and private funding is essential to convert mechanistic insight into broadly available treatments, to support expensive clinical trials, and to ensure equitable access to future therapies in low‑ and middle‑income countries.
The broader significance
Ultimately, the Nobel recognition highlights how curiosity‑driven science can create new medical paradigms: by revealing how the immune system is kept in check, the laureates have not only solved a fundamental biological riddle but also opened practical routes to treat diseases that affect millions worldwide, from autoimmune disorders to cancer and graft rejection.
