Abstract
Mouse liver contains both Eomes-dependent conventional natural killer (cNK) cells and Tbet-dependent liver-resident type I innate lymphoid cells (ILC1). In order to better understand the role of ILC1, we attempted to generate mice that would lack liver ILC1, while retaining cNK, by conditional deletion of Tbet in NKp46+ cells. Here we report that the Ncr1iCreTbx21fl/fl mouse has a roughly equivalent reduction in both the cNK and ILC1 compartments of the liver, limiting its utility for investigating the relative contributions of these two cell types in disease models. We also describe the phenotype of these mice with respect to NK cells, ILC1 and NKp46+ ILC3 in the spleen and small intestine lamina propria.
Highlights
Mouse liver contains two NK cell populations
We observed a reduction in the absolute number of conventional natural killer (cNK) in the liver (Figures 1C and D)
We had expected that this might be similar to the reduction of cNK in the spleen, but, at ~10-fold, it was more pronounced, potentially pointing towards a differential requirement for Tbet in cNK survival in or recruitment to the liver, compared to the spleen
Summary
Mouse liver contains two NK cell populations. Conventional NK cells (cNK) are defined by their expression of CD49b (DX5)[1], depend on the transcription factor Eomes[2], and circulate freely[1,3]. We crossed Tbx21fl/fl onto Ncr1iCre mice to produce conditional knockout (Ncr1iCre Tbx21fl/fl) animals, in which Tbet is lost only in NKp46+ cells.
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