When Fred Ramsdell, 64, was named a Nobel Prize winner earlier this week, he was deep in the Wyoming mountains, blissfully offline and surrounded by fresh snow. The next day, as he was wrapping up a three-week backpacking trip with his wife, her phone began to light up with hundreds of messages about the good news: Ramsdell, along with Mary E. Brunkow and Shimon Sakaguchi, had won the 2025 Nobel Prize in Physiology or Medicine for their discoveries that reshaped immunology. Ramsdell tells WIRED he was completely unaware that the Nobel Prizes were being announced, let alone that the Nobel committee was trying to get in touch with him. Sonoma Biotherapeutics, the biotechnology firm he co-founded, told reporters that Ramsdell was 'was living his best life and was off the grid on a preplanned hiking trip.' When the news finally reached him, Ramsdell says he was shocked. He knew that the work he and his colleagues did constituted a major breakthrough, but he had already received another Swedish award for it, and thus assumed a Nobel was out of the question....

Back in the 1980s, when Shimon Sakaguchi was a young researcher in immunology, he found it difficult to get his research funded. Now, his pioneering work which explains how our immune system knows when and what to attack, has won him a Nobel prize. Sakaguchi, along with American researchers Mary Brunkow and Fred Ramsdell, were jointly awarded the 2025 Nobel prize in physiology or medicine for their work on regulatory T-cells, known as T-regs for short, a special class of immune cells which prevent our immune system from attacking our own body. Sakaguchi was inspired by an experiment involving newborn mice conducted by his colleagues at the Aichi Cancer Center Research Institute in Nagoya. They'd removed the thymus from mice three days after they were born. It was already known that the thymus is important in the development of immune self-tolerance: it's where T-cells, a type of lymphocyte or white blood cell, that could attack the body are isolated and destroyed. Sakaguchi was intrigued by what happened. He said that if you remove the thymus in a normal mouse in the neonatal period, you would expect immune deficiency because the lymphocytes are gone....

Understanding how interactions between the central nervous system and the immune system contribute to problems of aging, including Alzheimer's disease, Parkinson's disease, arthritis, and more, can generate new leads for therapeutic development, speakers said at MIT's symposium 'The Neuro-Immune Axis and the Aging Brain' on Sept 18. 'The past decade has brought rapid progress in our understanding of how adaptive and innate immune systems impact the pathogenesis of neurodegenerative disorders,' said Picower Professor Li-Huei Tsai, director of The Picower Institute for Learning and Memory and MIT's Aging Brain Initiative (ABI), in her introduction to the event, which more than 450 people registered to attend. 'Together, today's speakers will trace how the neuro-immune axis shapes brain health and disease ' Their work converges on the promise of immunology-informed therapies to slow or prevent neurodegeneration and age-related cognitive decline.' For instance, keynote speaker Michal Schwartz of the Weizmann Institute in Israel described her decades of pioneering work to understand the neuro-immune 'ecosystem.' Immune cells, she said, help the brain heal, and support many of its functions, including its 'plasticity,' the ability it has to adapt to and incorporate new information. But Schwartz's lab also found that an immune signaling cascade can arise with aging that undermines cognitive function. She has leveraged that insight to investigate and develop corrective immunotherapies that improve the brain's immune response to Alzheimer's both by rejuvenating the brain's microglia immune cells and bringing in the help of peripheral immune cells called macrophages. Schwartz has brought the potential therapy to market as the chief science officer of ImmunoBrain, a company testing it in a clinical trial....

With discovery after discovery, Baltimore brought to light key features of biology with direct implications for human health. His work at MIT earned him a share of the 1975 Nobel Prize in Physiology or Medicine (along with Howard Temin and Renato Dulbecco) for discovering reverse transcriptase and identifying retroviruses, which use RNA to synthesize viral DNA. Following the award, Baltimore reoriented his laboratory's focus to pursue a mix of immunology and virology. Among the lab's most significant subsequent discoveries were the identification of a pair of proteins that play an essential role in enabling the immune system to create antibodies for so many different molecules, and investigations into how certain viruses can cause cell transformation and cancer. Work from Baltimore's lab also helped lead to the development of the important cancer drug Gleevec ' the first small molecule to target an oncoprotein inside of cells. In 1982, Baltimore partnered with philanthropist Edwin C. 'Jack' Whitehead to conceive and launch the Whitehead Institute and then served as its founding director until 1990. Within a decade of its founding, the Baltimore-led Whitehead Institute was named the world's top research institution in molecular biology and genetics....