Abstract
Abstract Tissue damage contributes to initiation and modulation of an immune response. Tumor progression generally causes distress to the surrounding tissue. However, how tumor-induced parenchymal damage regulates anti-tumor immune response remains to be understood. We found that tumors that invaded brain parenchyma compressed the surrounding neurons causing increased expression of the neuronal chemokine CX3CL1/fractalkine in the peritumoral margin. Intravital two-photon microscopy revealed perivascular recruitment of monocyte-derived CD11c+ dendritic cells and T cells that interacted and killed individual cancer cells in tumor margins. Immune surveillance of brain tumors became inefficient in mice lacking the receptor for fractalkine, CX3CR1, resulting in more aggressive tumor progression. Our results identify tissue stress and associated chemokine signaling as a potential target to orchestrate anti-tumor immune surveillance in the brain.
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