Innate lymphoid cells (ILCs) play a central role conferring protection at the mucosal frontier. In this study, we have identified a requirement of the transcription factor Zbtb1 for the development of RORγt ILCs (ILC3s). Zbtb1-deficient mice lacked NKp46 ILC3 cells in the lamina propria of the small and large intestine. This requirement of Zbtb1 was cell intrinsic, as NKp46 ILC3s were not generated from Zbtb1-deficient progenitors in bone marrow chimeras and Zbtb1-deficient RORγt CCR6NKp46 ILC3s didn't generate NKp46 ILC3s in co-cultures with OP9-DL1 stroma. In correlation with this impairment, Zbtb1-deficient ILC3 cells failed to upregulate T-bet expression, and to acquire IFN-γ production characteristic of NKp46 cells. Finally, absence of NKp46ILC3 cells combined with the absence of T-cells in Zbtb1-deficient mice, led to a transient susceptibility to infections. Altogether, these results establish that Zbtb1 is essential for the development of NKp46 ILC3 cells.
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| http://dx.doi.org/10.18632/oncotarget.19645 | DOI Listing |
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