| First Author | Dudeck J | Year | 2017 |
| Journal | J Exp Med | Volume | 214 |
| Issue | 12 | Pages | 3791-3811 |
| PubMed ID | 29084819 | Mgi Jnum | J:256207 |
| Mgi Id | MGI:6106494 | Doi | 10.1084/jem.20160783 |
| Citation | Dudeck J, et al. (2017) Mast cells acquire MHCII from dendritic cells during skin inflammation. J Exp Med 214(12):3791-3811 |
| abstractText | Mast cells (MCs) and dendritic cells (DCs) are essential innate sentinels populating host-environment interfaces. Using longitudinal intravital multiphoton microscopy of DC(GFP)/MC(RFP) 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. |
