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    Virus-Mediated Suppression of the Antigen Presentation Molecule MR1

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    Author
    McSharry, BP; Samer, C; McWilliam, HEG; Ashley, CL; Yee, MB; Steain, M; Liu, L; Fairlie, DP; Kinchington, PR; McCluskey, J; ...
    Date
    2020-03-03
    Source Title
    Cell Reports
    Publisher
    CELL PRESS
    University of Melbourne Author/s
    McCluskey, James; Villadangos, Jose; Rossjohn, Jamie; McWilliam, Hamish
    Affiliation
    Biochemistry and Molecular Biology
    Microbiology and Immunology
    Chancellery Research
    Metadata
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    Document Type
    Journal Article
    Citations
    McSharry, B. P., Samer, C., McWilliam, H. E. G., Ashley, C. L., Yee, M. B., Steain, M., Liu, L., Fairlie, D. P., Kinchington, P. R., McCluskey, J., Abendroth, A., Villadangos, J. A., Rossjohn, J. & Slobedman, B. (2020). Virus-Mediated Suppression of the Antigen Presentation Molecule MR1. CELL REPORTS, 30 (9), pp.2948-+. https://doi.org/10.1016/j.celrep.2020.02.017.
    Access Status
    Open Access
    URI
    http://hdl.handle.net/11343/252350
    DOI
    10.1016/j.celrep.2020.02.017
    NHMRC Grant code
    NHMRC/1113293
    Abstract
    The antigen-presenting molecule MR1 presents microbial metabolites related to vitamin B2 biosynthesis to mucosal-associated invariant T cells (MAIT cells). Although bacteria and fungi drive the MR1 biosynthesis pathway, viruses have not previously been implicated in MR1 expression or its antigen presentation. We demonstrate that several herpesviruses inhibit MR1 cell surface upregulation, including a potent inhibition by herpes simplex virus type 1 (HSV-1). This virus profoundly suppresses MR1 cell surface expression and targets the molecule for proteasomal degradation, whereas ligand-induced cell surface expression of MR1 prior to infection enables MR1 to escape HSV-1-dependent targeting. HSV-1 downregulation of MR1 is dependent on de novo viral gene expression, and we identify the Us3 viral gene product as functioning to target MR1. Furthermore, HSV-1 downregulation of MR1 disrupts MAIT T cell receptor (TCR) activation. Accordingly, virus-mediated targeting of MR1 defines an immunomodulatory strategy that functionally disrupts the MR1-MAIT TCR axis.

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