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    NLRC5 shields T lymphocytes from NK-cell-mediated elimination under inflammatory conditions

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    Author
    Ludigs, K; Jandus, C; Utzschneider, DT; Staehli, F; Bessoles, S; Dang, AT; Rota, G; Castro, W; Zehn, D; Vivier, E; ...
    Date
    2016-02-01
    Source Title
    Nature Communications
    Publisher
    NATURE PUBLISHING GROUP
    University of Melbourne Author/s
    Utzschneider, Daniel
    Affiliation
    Microbiology and Immunology
    Metadata
    Show full item record
    Document Type
    Journal Article
    Citations
    Ludigs, K., Jandus, C., Utzschneider, D. T., Staehli, F., Bessoles, S., Dang, A. T., Rota, G., Castro, W., Zehn, D., Vivier, E., Held, W., Romero, P. & Guarda, G. (2016). NLRC5 shields T lymphocytes from NK-cell-mediated elimination under inflammatory conditions. NATURE COMMUNICATIONS, 7 (1), https://doi.org/10.1038/ncomms10554.
    Access Status
    Open Access
    URI
    http://hdl.handle.net/11343/255880
    DOI
    10.1038/ncomms10554
    Abstract
    NLRC5 is a transcriptional regulator of MHC class I (MHCI), which maintains high MHCI expression particularly in T cells. Recent evidence highlights an important NK-T-cell crosstalk, raising the question on whether NLRC5 specifically modulates this interaction. Here we show that NK cells from Nlrc5-deficient mice exhibit moderate alterations in inhibitory receptor expression and responsiveness. Interestingly, NLRC5 expression in T cells is required to protect them from NK-cell-mediated elimination upon inflammation. Using T-cell-specific Nlrc5-deficient mice, we show that NK cells surprisingly break tolerance even towards 'self' Nlrc5-deficient T cells under inflammatory conditions. Furthermore, during chronic LCMV infection, the total CD8(+) T-cell population is severely decreased in these mice, a phenotype reverted by NK-cell depletion. These findings strongly suggest that endogenous T cells with low MHCI expression become NK-cell targets, having thus important implications for T-cell responses in naturally or therapeutically induced inflammatory conditions.

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