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    Dendritic Cell-Mediated Phagocytosis but Not Immune Activation Is Enhanced by Plasmin.

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    Author
    Borg, RJ; Samson, AL; Au, AE-L; Scholzen, A; Fuchsberger, M; Kong, YY; Freeman, R; Mifsud, NA; Plebanski, M; Medcalf, RL
    Date
    2015
    Source Title
    PLoS One
    Publisher
    Public Library of Science (PLoS)
    University of Melbourne Author/s
    Au, Amanda
    Affiliation
    Medical Biology (W.E.H.I.)
    Metadata
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    Document Type
    Journal Article
    Citations
    Borg, R. J., Samson, A. L., Au, A. E. -L., Scholzen, A., Fuchsberger, M., Kong, Y. Y., Freeman, R., Mifsud, N. A., Plebanski, M. & Medcalf, R. L. (2015). Dendritic Cell-Mediated Phagocytosis but Not Immune Activation Is Enhanced by Plasmin.. PLoS One, 10 (7), pp.e0131216-. https://doi.org/10.1371/journal.pone.0131216.
    Access Status
    Open Access
    URI
    http://hdl.handle.net/11343/253445
    DOI
    10.1371/journal.pone.0131216
    Open Access at PMC
    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4488505
    Abstract
    Removal of dead cells in the absence of concomitant immune stimulation is essential for tissue homeostasis. We recently identified an injury-induced protein misfolding event that orchestrates the plasmin-dependent proteolytic degradation of necrotic cells. As impaired clearance of dead cells by the innate immune system predisposes to autoimmunity, we determined whether plasmin could influence endocytosis and immune cell stimulation by dendritic cells - a critical cell that links the innate and adaptive immune systems. We find that plasmin generated on the surface of necrotic cells enhances their phagocytic removal by human monocyte-derived dendritic cells. Plasmin also promoted phagocytosis of protease-resistant microparticles by diverse mouse dendritic cell sub-types both in vitro and in vivo. Together with an increased phagocytic capacity, plasmin-treated dendritic cells maintain an immature phenotype, exhibit reduced migration to lymph nodes, increase their expression/release of the immunosuppressive cytokine TGF-β, and lose their capacity to mount an allogeneic response. Collectively, our findings support a novel role for plasmin formed on dead cells and other phagocytic targets in maintaining tissue homeostasis by increasing the phagocytic function of dendritic cells while simultaneously decreasing their immunostimulatory capacity consistent with producing an immunosuppressive state.

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