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

Kristina Ludigs, Camilla Jandus, Daniel T. Utzschneider, Francesco Staehli, Stéphanie Bessoles, Anh Thu Dang, Giorgia Rota, Wilson Castro, Dietmar Zehn, Eric Vivier, Werner Held, Pedro Romero and Greta Guarda ()
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Kristina Ludigs: University of Lausanne
Camilla Jandus: Ludwig Center for Cancer Research of the University of Lausanne
Daniel T. Utzschneider: CHUV, University of Lausanne
Francesco Staehli: University of Lausanne
Stéphanie Bessoles: Ludwig Center for Cancer Research of the University of Lausanne
Anh Thu Dang: University of Lausanne
Giorgia Rota: University of Lausanne
Wilson Castro: University of Lausanne
Dietmar Zehn: CHUV, University of Lausanne
Eric Vivier: Centre d’Immunologie de Marseille-Luminy, Aix-Marseille University UM2
Werner Held: Ludwig Center for Cancer Research of the University of Lausanne
Pedro Romero: Ludwig Center for Cancer Research of the University of Lausanne
Greta Guarda: University of Lausanne

Nature Communications, 2016, vol. 7, issue 1, 1-10

Abstract: 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.

Date: 2016
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DOI: 10.1038/ncomms10554

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