| dc.identifier.citation | 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. | |
| dc.description.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. | |
