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In a new study led by Professor Mike Dustin at the Kennedy Institute, and the team lead Dr. Alexander Leithner (now at the University of Salzburg, Austria), in collaboration with Audun Kvalvaag, at the Institute for Cancer Research at the University Hospital Oslo, examined how the physical presentation of a protein called ICAM-1 (Intercellular Adhesion Molecule 1) on a target cells affects the activation of T cells — the immune system’s cells responsible for identifying and eliminating infected or cancerous cells.
Published in PNAS, their findings show that when ICAM-1 is locked in place, rather than free to move within the cell membrane, T cells show a stronger response and become more effective at killing target cells. The study provides new insight that could help design better immune strategies and may have implications for vaccine design, cancer immunotherapy and understanding immune evasion.
Proteins on the surface of cells are not fixed. Many float freely within the fluid lipid membrane of the cell’s outer layer. However, some proteins such as ICAM-1 can be locked in place by attaching to the underlying cell skeleton or cytoskeleton.
ICAM-1 is found on antigen-presenting cells, specialist immune cells which activate T cells by showing them fragments of pathogens or tumours. Previous research has shown that ICAM-1 tends to float freely on less effective antigen-presenting cells but is anchored to the cytoskeleton in the best performing ones.