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.

肥大细胞（MC）和树突状细胞（DC）是必不可少的先天前哨，构成宿主-环境界面。使用纵向活体多光子显微镜观察DC ^GFP / MC ^RFP记者小鼠，我们在这里提供体内证据，表明迁徙性DC在离开发炎的皮肤至引流淋巴结之前执行与固定MC的定向细胞间相互作用。在皮肤发炎的初始阶段，DC会动态扫描MC，而在以后的阶段中，持久的交互作用占主导。这些先天到先天的突触样接触最终在DC-MC分子转移（包括主要的组织相容性复合体II类（MHCII）蛋白）中达到高潮，从而能够随后以特定的细胞因子签名对同种异体T细胞进行离体启动。MHCII转移到MC的程度与其T细胞启动效率相关。重要的是，通过防止DC耗尽来防止串扰会降低MC抗原的呈递能力和T细胞驱动的炎症。所以，