Nobel Medicine Prize 2025
Kartavya Desk Staff
Source: HT
Context: The 2025 Nobel Prize in Physiology or Medicine was awarded to Mary E. Brunkow, Frederick J. Ramsdell, and Shimon Sakaguchi for discoveries on peripheral immune tolerance.
About Nobel Medicine Prize 2025:
What it is?
• The world’s top biomedical award, conferred by the Nobel Assembly at Karolinska Institute; prize money ~SEK 11 million and a gold medal.
Winners:
• Shimon Sakaguchi (Osaka University, Japan)
• Mary E. Brunkow (Institute for Systems Biology, USA)
• Frederick J. Ramsdell (Sonoma Biotherapeutics, USA)
Their Work:
• Regulatory T Cells (Tregs) and Peripheral Tolerance
• In 1995, Shimon Sakaguchi discovered a special kind of immune cell — regulatory T cells, or Tregs — that act like police officers of the immune system. These cells stop other immune cells from attacking the body’s own healthy tissues. When the thymus (an immune organ) was removed in baby mice, they developed autoimmune diseases, but when normal T cells were added back, they became healthy again — proving such “policing” cells exist.
• In 1995, Shimon Sakaguchi discovered a special kind of immune cell — regulatory T cells, or Tregs — that act like police officers of the immune system.
• These cells stop other immune cells from attacking the body’s own healthy tissues. When the thymus (an immune organ) was removed in baby mice, they developed autoimmune diseases, but when normal T cells were added back, they became healthy again — proving such “policing” cells exist.
• FOXP3 — The Master Control Gene of Tregs
• Scientists Mary Brunkow and Fred Ramsdell studied “scurfy” mice that developed severe autoimmune diseases and found a single faulty gene called FOXP3 caused it. This gene acts like a switch — turning normal T cells into regulatory ones. Without FOXP3, Tregs can’t form, and the body starts attacking itself, leading to autoimmune disorders like IPEX syndrome in humans.
• Scientists Mary Brunkow and Fred Ramsdell studied “scurfy” mice that developed severe autoimmune diseases and found a single faulty gene called FOXP3 caused it.
• This gene acts like a switch — turning normal T cells into regulatory ones. Without FOXP3, Tregs can’t form, and the body starts attacking itself, leading to autoimmune disorders like IPEX syndrome in humans.
• Peripheral Immune Tolerance
• The immune system has two levels of control: “central tolerance” (inside the thymus, where bad cells are removed) and “peripheral tolerance” (in the rest of the body). Tregs are key to peripheral tolerance — they constantly guard tissues, prevent unnecessary inflammation, and stop the immune system from going out of control.
• The immune system has two levels of control: “central tolerance” (inside the thymus, where bad cells are removed) and “peripheral tolerance” (in the rest of the body).
• Tregs are key to peripheral tolerance — they constantly guard tissues, prevent unnecessary inflammation, and stop the immune system from going out of control.
Scientific Significance:
• Cancer therapy: Many tumors recruit Tregs to shield themselves. Strategies that deplete or disable Tregs in the tumor microenvironment can boost anti-tumor immunity and improve checkpoint inhibitors or CAR-T outcomes.
• Autoimmune diseases: Expanding or engineering Tregs (e.g., FOXP3+ Treg cell therapies) offers targeted ways to calm pathogenic immunity in conditions like type 1 diabetes, IBD, MS, and lupus.
• Transplantation & tolerance: Treg-based approaches may reduce long-term immunosuppression, lowering infection and toxicity risks after organ or cell transplants.
• Diagnostics & biomarkers: FOXP3 and Treg signatures aid disease stratification, response prediction, and trial design.
• Balanced risk awareness: Inhibiting Tregs can unmask autoimmunity; boosting Tregs may increase risks of infection or tumor escape—guiding safer, precision dosing and monitoring.