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    The receptor DNGR-1 signals for phagosomal rupture to promote cross-presentation of dead-cell-associated antigens

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    Authors
    Canton, J.
    Blees, H.
    Henry, C. M.
    Buck, M. D.
    Schulz, O.
    Rogers, N. C.
    Childs, E.
    Zelenay, Santiago
    Rhys, H.
    Domart, M. C.
    Collinson, L.
    Alloatti, A.
    Ellison, C. J.
    Amigorena, S.
    Papayannopoulos, V.
    Thomas, D. C.
    Randow, F.
    Reis, E. S. C.
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    Affiliation
    Immunobiology Laboratory, The Francis Crick Institute, London
    Issue Date
    2020
    
    Metadata
    Show full item record
    Abstract
    Type 1 conventional dendritic (cDC1) cells are necessary for cross-presentation of many viral and tumor antigens to CD8+ T cells. cDC1 cells can be identified in mice and humans by high expression of DNGR-1 (also known as CLEC9A), a receptor that binds dead-cell debris and facilitates XP of corpse-associated antigens. Here, we show that DNGR-1 is a dedicated XP receptor that signals upon ligand engagement to promote phagosomal rupture. This allows escape of phagosomal contents into the cytosol, where they access the endogenous major histocompatibility complex class I antigen processing pathway. The activity of DNGR-1 maps to its signaling domain, which activates SYK and NADPH oxidase to cause phagosomal damage even when spliced into a heterologous receptor and expressed in heterologous cells. Our data reveal the existence of innate immune receptors that couple ligand binding to endocytic vesicle damage to permit MHC class I antigen presentation of exogenous antigens and to regulate adaptive immunity.
    Citation
    Canton J, Blees H, Henry CM, Buck MD, Schulz O, Rogers NC, et al. The receptor DNGR-1 signals for phagosomal rupture to promote cross-presentation of dead-cell-associated antigens. Nat Immunol. 2020.
    Journal
    Nature Immunology
    URI
    http://hdl.handle.net/10541/623737
    DOI
    10.1038/s41590-020-00824-x
    PubMed ID
    33349708
    Additional Links
    https://dx.doi.org/10.1038/s41590-020-00824-x
    Type
    Article
    Language
    en
    ae974a485f413a2113503eed53cd6c53
    10.1038/s41590-020-00824-x
    Scopus Count
    Collections
    All Paterson Institute for Cancer Research

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