Sports & AwardsPriority2025-10-06

2025 Nobel Prize in Physiology or Medicine Awarded

Why focus: Nobel in Medicine for Regulatory T cells — perfect GS3 Sci-Tech proxy for human immune system concepts linked to NCERT Class 12 Biology.

In News

What Happened

On October 6, 2025, Mary E. Brunkow, Fred Ramsdell, and Shimon Sakaguchi were jointly awarded the Nobel Prize in Physiology or Medicine. They were recognized for their discovery of regulatory T cells and the FOXP3 gene, which act as the immune system's security guards to prevent the body from attacking its own tissues.

Why It Matters

This breakthrough fundamentally explains how our body maintains 'peripheral immune tolerance', preventing deadly autoimmune diseases like Type 1 diabetes and rheumatoid arthritis. It also forms the basis for cutting-edge medical treatments, such as boosting tolerance to prevent organ transplant rejection or suppressing it so the immune system can attack cancer tumors.

Background

History & Context

Historically, immunologists believed that the body prevented autoimmunity solely by destroying self-reacting immune cells during their development in the thymus gland, a process called central tolerance. However, this theory could not explain why some self-reactive cells escape the thymus without causing disease. In 1995, Shimon Sakaguchi swam against the scientific tide by identifying a specific subpopulation of T cells in the peripheral bloodstream that actively suppress immune responses. Concurrently, Mary Brunkow and Fred Ramsdell were studying 'scurfy' mice, an evolutionary fluke strain suffering from a fatal autoimmune disease. In 2001, Brunkow and Ramsdell mapped the genetic cause to a newly identified gene they named Foxp3, and linked its human equivalent to a severe autoimmune disorder known as IPEX syndrome. By 2003, Sakaguchi connected these two streams of research, proving that the FOXP3 gene is the master regulator that governs the development of regulatory T cells.

What Changed

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BEFORE: Central immune tolerance (thymic deletion of immune cells) was considered the only major mechanism for preventing autoimmunity. NOW: Peripheral immune tolerance, mediated actively by regulatory T cells (Tregs) circulating in the body, is recognized as an essential, ongoing mechanism.
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BEFORE: The genetic cause of the fatal autoimmune condition in 'scurfy' mice and the severe human IPEX syndrome was a complete mystery. NOW: The FOXP3 gene was identified as the direct genetic driver, proving that a single gene mutation can dismantle immune tolerance.
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BEFORE: Immune system T cells were broadly understood as either 'helpers' (CD4+) or 'killers' (CD8+) that activate to fight pathogens. NOW: A distinct subset of 'suppressor' or regulatory T cells (CD4+CD25+FOXP3+) is known to actively dampen and turn off immune reactions.
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BEFORE: Cancer and autoimmune therapies largely relied on broad, systemic immunosuppression or non-specific stimulation. NOW: Targeted therapies are being developed to precisely inhibit Tregs (allowing the immune system to destroy cancer cells) or boost Tregs (to treat autoimmune diseases and prevent organ transplant rejection).

What Did NOT Change

Despite these targeted discoveries, the fundamental reality that the immune system must continuously balance attack and tolerance remains the same. Additionally, while Treg-specific therapies have entered clinical trials, traditional broad immunosuppressive drugs are still widely used as the standard of care for many autoimmune conditions.

Prelims Angle

NCERT Connection

This connects directly to Class 12 Biology, Chapter 8 (Human Health and Disease), specifically the sections on Immunity and Autoimmunity. The NCERT textbook explains that higher vertebrates evolved memory-based acquired immunity to distinguish foreign molecules from self-cells, and that when this 'self vs. non-self' recognition fails, autoimmune diseases result. The 2025 Nobel Prize discovery provides the specific cellular and genetic mechanism (Regulatory T cells and the FOXP3 gene) that mediates this tolerance in the real world.

Common Misconceptions

✗ T cells are exclusively involved in attacking foreign pathogens or virally infected cells.

✓ A specific subset called Regulatory T cells (Tregs) actively suppress the immune response and prevent other T cells from attacking healthy host tissues.

Basic biology education heavily focuses on Cytotoxic T cells (killers) and Helper T cells, often omitting the suppressive role of Tregs.

✗ The body prevents autoimmunity only by destroying bad immune cells before they mature in the thymus.

✓ Self-reactive immune cells frequently escape the thymus, but peripheral tolerance via Tregs keeps them in check in the bloodstream and tissues.

Central tolerance (in the thymus) is an older, easier-to-teach concept, leading to the assumption that peripheral checkpoints do not exist.

Practice Questions

Q1

How Many Correct

Consider the following statements regarding Regulatory T cells (Tregs) and peripheral immune tolerance: 1. Shimon Sakaguchi discovered that Tregs actively suppress the immune system to prevent autoimmune diseases. 2. The FOXP3 gene acts as the master transcription factor for the development of regulatory T cells. 3. Central immune tolerance occurs in the peripheral blood, whereas peripheral tolerance occurs in the thymus. How many of the above statements are correct?

Q2

Match the Following

Match the following terms related to the 2025 Nobel Prize in Medicine with their descriptions: List I: A. FOXP3, B. IPEX Syndrome, C. Central Tolerance, D. Scurfy mice. List II: 1. Elimination of self-reactive T cells in the thymus, 2. Animal model with a fatal autoimmune defect, 3. Human autoimmune disease caused by a specific gene mutation, 4. Transcription factor essential for Regulatory T cell development.

Q3

Assertion & Reason

Assertion (A): Mutations in the human FOXP3 gene lead to the severe autoimmune disorder known as IPEX syndrome. Reason (R): The FOXP3 gene encodes a transcription factor that programs T-cells to become Cytotoxic T-cells, which destroy self-tissues. Select the correct answer.

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