The Rudensky Symposium on Immunity, Inflammation and Tolerance, held on August 27–28, 2026, was more than a typical scientific meeting. Celebrating the 70th birthday of Alexander “Sasha” Rudensky, PhD, of Memorial Sloan Kettering Cancer Center, the symposium brought together former trainees, collaborators, and colleagues whose relationships spanned decades. Scientific presentations were interwoven with shared memories, reflecting the mentorship and friendships that had shaped their lives and careers.
The Cancer Research Institute (CRI) was proud to support this symposium and celebrate a member of its Scientific Advisory Council (SAC). For more than 20 years, CRI has backed Dr. Rudensky’s research and mentorship, including over a dozen CRI-funded fellows who have moved through his lab. In 2015, he received the CRI William B. Coley Award for pioneering work on regulatory T cells, or Tregs, immune cells that restrain excessive responses and help protect healthy tissues from damage.
CRI’s connections to this scientific community run deep, reflecting a longstanding commitment to funding basic immunology alongside cancer immunology. That support recognizes that understanding how the immune system works is fundamental to learning how to harness it against cancer.
Across discussions of tissue repair, the gut microbiome, immune tolerance, and cancer, a common thread emerged: the processes that keep healthy tissues in balance also shape how cancer develops, spreads, and responds to treatment. Understanding those connections is opening new directions for cancer prevention and therapy, often from discoveries that began with a different biological question.
Basic Science Reveals How Tissues Stay In Balance
Some of the talks at the symposium began with questions not explicitly about cancer, but revealed principles relevant to cancer research. CRI scientist and 2003 CRI Coley Awardee, Ruslan Medzhitov, PhD, described how stressed cells may recruit macrophages to remove damaged protein “garbage,” suggesting that immune cells serve as tissue maintenance crews as well as defenders against infection.
The symposium highlighted that Tregs also have roles that extend beyond suppressing immune responses. Diane Mathis, PhD, described populations that help injured muscle control inflammation, guide repair, and limit scarring. Christophe Benoist, MD, PhD, showed that the molecular target a Treg recognizes can help determine its identity and function. Both scientists received the 2024 CRI Coley Award.
These insights matter because immune restraint must be precise. Too little can contribute to autoimmunity and tissue damage. Too much can help cancer escape.
Can Immunity Act Before Cancer Takes Hold?
CRI scientist and 2012 CRI Coley Awardee Richard A. Flavell, PhD, explored how early cancer immunosurveillance might begin by studying mutant intestinal stem cells before a visible tumor exists. In mouse models, cells carrying a cancer-linked BRAF mutation gained a competitive survival advantage, but many were still eliminated.
These experiments suggested that immune recognition helps determine which abnormal cells survive early. When mutant cells lost a molecule involved in communicating with T cells, they were more likely to take over the small compartments where intestinal stem cells reside. Tregs and the immune signal IL-10 also appeared to help restrain these early clones.
The work is preclinical, but the concept is powerful: the immune system may influence cancer development from the moment a potentially dangerous cell begins competing with its normal neighbors.
Julien C. Marie, PhD, approached the inflammation-cancer connection from another direction. In mice, disrupting a regulatory signal called TGF-β pushed intestinal Th17 cells, a type of immune cell, into a persistently inflammatory state associated with localized DNA damage and eventual cancer development. Restoring the signal reversed aspects of that state, suggesting harmful inflammatory programs may retain some flexibility.
Cancer Depends On Its Wider Ecosystem
CRI SAC member and 2016 CRI Coley Awardee, Dan Littman, MD, PhD, connected the gut microbiome to cancer immunotherapy. His preclinical work explored how gut bacteria train T cells and influence responses to checkpoint immunotherapy, illustrating how an immune response beginning in the intestine can affect cancer elsewhere in the body.
Paula D. Bos, PhD, showed how Tregs can affect breast cancer through macrophages and the physical scaffolding surrounding a tumor. Temporarily removing Tregs in mouse tumors shifted macrophages toward a tumor-fighting state and disrupted aligned collagen fibers that can act like highways for cancer-cell escape. The mice subsequently had fewer circulating tumor cells and less metastatic disease.
The goal is not to broadly eliminate Tregs, which could cause harmful immune responses. Instead, these experiments can reveal more specific ways to influence macrophage behavior and tumor spread.
Nicholas Arpaia, PhD, also examined how tumors create immune-suppressive neighborhoods. His group identified a fibroblast population that attracts suppressive Tregs around lung tumors. He also described work developed with CRI Lloyd J. Old STAR Tal Danino, PhD, using engineered bacteria to deliver therapies inside tumors. The broader goal is to concentrate immune-modulating treatments where they are needed.
Progress Begins With People
The Rudensky Symposium showed how advances in cancer research grow from basic questions about immune cells, tissues, and their interactions. It also showed how progress depends on mentorship, collaboration, rigorous disagreement, and the freedom to pursue questions whose clinical relevance may not be obvious at first.
Rudensky Symposium poster board signed by Dr. Rudensky’s Research Family.
Photo courtesy of the author
Seeing generations of scientists gathered in one room made that ripple effect tangible. For more than 70 years, CRI has invested in this foundation of discovery, supporting the science and the people who carry it forward. The symposium brought that long-term commitment to life: trainees becoming mentors, discoveries informing new fields, and collaborations connecting fundamental questions to the shared goal of improving patients’ lives.
