期刊
ONCOTARGET
卷 8, 期 34, 页码 55877-55888出版社
IMPACT JOURNALS LLC
DOI: 10.18632/oncotarget.19645
关键词
innate lymphoid cells; ILC; ILC3; Zbtb1; IFN-gamma; Immunology and Microbiology Section; Immune response; Immunity
资金
- NIH intramural funds [1ZIABC011429]
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 ROR gamma t(+) 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 ROR gamma t(+) CCR6-NKp46-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-gamma production characteristic of NKp46(+) cells. Finally, absence of NKp46(+) ILC3 cells combined with the absence of T-cells in Zbtb1-deficient mice, led to a transient susceptibility to C. rodentium infections. Altogether, these results establish that Zbtb1 is essential for the development of NKp46(+) ILC3 cells.
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