Dendritic cells have a sweet tooth

Dendritic cells serve as messengers between our body’s first line of defense (the innate immune system) and the adaptive immune system, which provides long-term immunity. To effectively trigger an immune response, dendritic cells rely on the migratation from the peripheral tissues into lymph nodes - a journey that depends on their ability to polarize (establish a front and a back) and move directionally. Disruption of dendritic cell migration can lead to immune system malfunctions, contributing to chronic inflammation or ineffective immune responses to cancer. However, the molecular players involved in this process are poorly understood.

Research led by Laia Querol Cano, from the Department of Medical BioSciences at Radboud university medical center, in collaboration with Radboud University and Brunel University London, has uncovered that a sugar-binding protein named galectin-9 is required for proper dendritic cell migration. Using dendritic cells isolated from human and mouse blood, genetic models and advanced imaging, Guus Franken, Harry Warner and Jorge Cuenca-Escalona discovered that in the absence of galectin-9, dendritic cells failed to maintain a proper orientation, exhibiting an abnormal morphology together with adefective capacity toto migrate under (patho)-physiological circumstances.

Why this matters: Proper dendritic cell function is vital for immunity, as these cells activate T cells to target infections and kill tumour cells. If dendritic cells cannot reach lymph nodes or tumour sites, immune activation is blunted.

Next steps will delve into how modulating galectin-9 activity could be exploited to finetune the function of dendritic cells for therapeutic purposes.. For example, we hypothesize that enhancing galectin-9 signaling will aid to recover the impaired function of dendritic cells in cancer, opening up new venues in the search for better treatments in the fight against cancer.

Findings were published in Journal of Cell Biology 24 November 2025.