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Mast cells acquire MHC II from dendritic cells during skin inflammation.

J. Exp. Med. 214, 3791-3811 (2017)
Publishers Version DOI
Open Access Gold (Paid Option)
Creative Commons Lizenzvertrag
as soon as is submitted to ZB.
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.
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Publication type Article: Journal article
Document type Scientific Article
Keywords Allergic Contact-dermatitis; Cd8(+) T-cells; Class-ii; Elicitation Phase; In-vivo; Responses; Antibody; Hypersensitivity; Complexes; Immunity
Reviewing status
Institute(s) Institute for Pancreatic Beta Cell Research (IPI)