NLRC5 shields T lymphocytes from NK-cell-mediated elimination under inflammatory conditions
AuthorLudigs, K; Jandus, C; Utzschneider, DT; Staehli, F; Bessoles, S; Dang, AT; Rota, G; Castro, W; Zehn, D; Vivier, E; ...
Source TitleNature Communications
PublisherNATURE PUBLISHING GROUP
University of Melbourne Author/sUtzschneider, Daniel
AffiliationMicrobiology and Immunology
Document TypeJournal Article
CitationsLudigs, 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 StatusOpen Access
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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