TY  - JOUR
AU  - Ludigs, K
AU  - Jandus, C
AU  - Utzschneider, DT
AU  - Staehli, F
AU  - Bessoles, S
AU  - Dang, AT
AU  - Rota, G
AU  - Castro, W
AU  - Zehn, D
AU  - Vivier, E
AU  - Held, W
AU  - Romero, P
AU  - Guarda, G
Y2  - 2020/12/18
Y1  - 2016/02/01
SN  - 2041-1723
UR  - http://hdl.handle.net/11343/255880
AB  - 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.
LA  - English
PB  - NATURE PUBLISHING GROUP
T1  - NLRC5 shields T lymphocytes from NK-cell-mediated elimination under inflammatory conditions
DO  - 10.1038/ncomms10554
IS  - Nature Communications
VL  - 7
IS  - 1
L1  - /bitstream/handle/11343/255880/PMC4749981.pdf?sequence=1&isAllowed=y
ER  -