ILC1 quiescence confers protection against MCMV infections during undernutrition
In the liver, group 1 innate lymphoid cells (ILCs) comprise 10–20% tissue-resident ILC1 cells and 80–90% conventional NK cells. Both cells contribute to early defense against virus infection by secreting IFN-?. However, the distinct role of ILC1 cells in viral infections remains incompletely understood. Here, we identified that ILC1 cells outnumbered NK cells, constituting 80–90% of group 1 ILCs in the liver during undernutrition. Mechanistically, undernutrition significantly reduced NK cell numbers, while hepatic ILC1 cells entered a quiescent state that allowed them to survive in an mTORC1-dependent manner. Metabolically, quiescent ILC1 cells exhibited greater glucose uptake than NK cells and efficiently utilized it via oxidative phosphorylation, which was induced by mTORC1. Finally, ILC1-deficient mice succumbed to MCMV infection under undernourished conditions, but not when fed ad libitum. These findings suggest a non-redundant function of hepatic ILC1 cells in protecting the host against MCMV infection during undernutrition. Overall design: RNA-seq profiling of NK cells and ILC1 cells from wild type mice and Rptor flox Ncr1-Cre mice fed ad libitum or calorie-restricted.