Mar 15 • 01:00 UTC 🇯🇵 Japan Asahi Shimbun (JP)

Control T-cell Paper Published in Nature: Overcoming Adverse Winds in Academia

Professor Shimon Sakaguchi of Osaka University discusses the challenges he faced in T-regulatory cell research and the eventual recognition of his work despite initial skepticism.

Professor Shimon Sakaguchi from Osaka University, who was awarded the Nobel Prize in Physiology or Medicine for 2025, shared insights on his journey in T-regulatory cell research amidst adversity. In a conversation with his long-standing friend, Professor Shinichi Nishikawa from Kyoto University, and his wife, Kyoko Sakaguchi, they highlighted the early periods in Sakaguchi's career, including his study period in the US where he secured a scholarship but faced a lack of attention for his research. The initial hypothesis of "suppressor T-cells" in the 1970s gained traction, yet the reality was never confirmed, leading to a phase of skepticism beginning around 1983.

Sakaguchi faced significant challenges as his work on T-regulatory cells, which are distinct from the previously troubling suppressor T-cells, faced adverse winds. He focused on identifying unique markers and found that T-cells expressing both CD4 and CD25 are crucial for suppressing autoimmune diseases. His groundbreaking findings led to the publication of a pivotal paper in 1995 that enabled the confirmation of the existence of T-regulatory cells. Despite the importance of this research, it was not published in prestigious journals like Nature but rather in the Journal of Immunology after being rejected multiple times.

The discussion revealed the resistance Sakaguchi faced from prominent figures in immunology, notably Ethan Shevach from the NIH, who had a strong bias against the concept of suppressor T-cells. Sakaguchi's work eventually challenged existing beliefs and emphasized the need for recognition of T-regulatory cells in the scientific community, marking a significant milestone in immunology and potentially altering treatment approaches for autoimmune diseases.

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