Dendritic cells are highly sensitive to the mechanical cues in their surroundings. A special niche for mechanical stimuli is the tumor and its microenvironment, where both extracellular matrix organization and stiffness of tumor cells themselves could contribute to the mechanical stimulation of DCs. We observed that interferon gamma (IFNγ), a cytokine that becomes predominant when primed T cells infiltrate tumors, increases the levels of filamentous actin and cortex thickness of tumor cells. This finding suggests that IFNγ could modify their mechanical properties and thus the way tumor cells interact with DCs. To address this question, we co-cultured DCs together with tumor cells previously stimulated or not with IFNγ. Surprisingly, we observed that DCs can form “cell-in-cell structures” with tumor cells, especially in the presence of IFNγ. This phenomenon is reminiscent of “emperipolesis”, which has been described for other cell types. Live-imaging experiments revealed that DCs actively penetrate tumor cells and can then follow distinct fates. They can either remain within tumor cells for long time-periods wherein they divide and/or progressively lose their integrity, suggesting they might constitute a food and energy source for tumor cells. Alternatively, DCs can exit from tumor cells in a live-state and keep patrolling the environment. Our preliminary results suggest that emperipolesis is not observed when macrophages -rather that DCs- are co-cultured with tumor cells. Our current objectives are to (1) unravel the underlying mechanisms of DC-tumor cell emperipolesis, and (2) its putative role in tumor antigen acquisition by DCs and regulation by IFNγ.