Mast cells acquire MHCII from dendritic cells during skin inflammation.

Dudeck J*, Medyukhina A*, Froebel J, Svensson C-M, Kotrba J, Gerlach M, Gradtke AC, Schröder B, Speier S, Figge MT**, Dudeck A**; *authors contributed equally; **corresponding authors, authors contributed equally (2017) Mast cells acquire MHCII from dendritic cells during skin inflammation. J Exp Med 214(12), 3791-3811.

*equal contribution


Mast cells (MCs) and dendritic cells (DCs) are essential innate sentinels populating host-environment interfaces. Using longitudinal intravital multiphoton microscopy of DCGFP/MCRFP reporter mice, we herein provide in vivo evidence that migratory DCs execute targeted cell-to-cell interactions with stationary MCs before leaving the inflamed skin to draining lymph nodes. During initial stages of skin inflammation, DCs dynamically scan MCs, whereas at a later stage, long-lasting interactions predominate. These innate-to-innate synapse-like contacts ultimately culminate in DC-to-MC molecule transfers including major histocompatibility complex class II (MHCII) proteins enabling subsequent ex vivo priming of allogeneic T cells with a specific cytokine signature. The extent of MHCII transfer to MCs correlates with their T cell priming efficiency. Importantly, preventing the cross talk by preceding DC depletion decreases MC antigen presenting capacity and T cell–driven inflammation. Consequently, we identify an innate intercellular communication arming resident MCs with key DC functions that might contribute to the acute defense potential during critical periods of migration-based DC absence.


Marc Thilo Figge
Anna Medyukhina
Carl-Magnus Svensson


doi: 10.1084/jem.20160783

PMID: 29084819