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New Immune Mechanism Linked to Duodenal Cancer Risk in FAP Patients

Research identifies IL-17A-producing ILC3 cells as drivers of oxidative DNA damage, pointing to immunomodulation as a preventive strategy.

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Overview

  • A study published in *Nature Communications* reveals that type 3 innate lymphoid cells (ILC3) are present in higher numbers in the duodenum of familial adenomatous polyposis (FAP) patients.
  • These ILC3 cells produce interleukin-17A (IL-17A), which induces the production of reactive oxygen species (ROS) in intestinal cells, leading to oxidative DNA damage.
  • The local accumulation of IL-17A-producing ILC3 creates a pro-carcinogenic environment in the duodenal mucosa, increasing cancer risk in FAP patients.
  • Researchers suggest that targeting ILC3 cells or blocking IL-17A directly in the duodenum could serve as a novel preventive approach to complement existing endoscopic surveillance.
  • This discovery highlights the role of the immune microenvironment in modulating FAP severity and introduces immunomodulation as a potential addition to current clinical management strategies.