Mast cells acquire MHCII from dendritic cells during skin inflammation
Mast cells acquire MHCII from dendritic cells during skin inflammation
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DOI：
10.1084/jem.20160783
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发表时间：
2017-12-01
影响因子：
15.3
通讯作者：
Dudeck, Anne
中科院分区：
文献类型：
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作者：
Dudeck, Jan;Medyukhina, Anna;Dudeck, Anne
肥大细胞（MC）和树突状细胞（DCs）是宿主-环境界面的重要天然哨兵。使用DCGFP/MCRFP报告小鼠的纵向活体多光子显微镜，我们在此提供了体内证据，证明迁移性DC在离开发炎皮肤至引流淋巴结之前与静止MC进行靶向细胞间相互作用。在皮肤炎症的初始阶段，DC动态扫描MC，而在后期，持久的相互作用占主导地位。这些先天性与先天性突触样接触最终导致DC至MC分子转移，包括主要组织相容性复合物II类（MHCII）蛋白，使得能够随后用特异性细胞因子特征离体引发同种异体T细胞。MHCII转移到MC的程度与其T细胞引发效率相关。重要的是，通过预先消耗DC来防止串扰会降低MC抗原呈递能力和T细胞驱动的炎症。因此，我们确定了一种先天的细胞间通讯武装居民MC与关键的DC功能，可能有助于急性防御潜力在关键时期的迁移为基础的DC缺席。
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.