1. PLZF restricts intestinal ILC3 function in gut defense.
- Author
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Xu Y, Zhang H, Wu S, Liu J, Liu H, Wang D, Zhang Y, Niu H, Su X, Sun J, and Shen L
- Subjects
- Humans, Gene Expression, Inflammation metabolism, Transcription Factors metabolism, Immunity, Innate, Lymphocytes, Promyelocytic Leukemia Zinc Finger Protein metabolism
- Abstract
Group 3 innate lymphoid cells (ILC3s) play important roles in maintaining intestinal homeostasis by protecting the host from pathogen infections and tissue inflammation. The transcription factor PLZF (promyelocytic leukemia zinc finger), encoded by zinc finger BTB domain containing 16 (Zbtb16), is highly and transiently expressed in ILC precursors (ILCPs). However, the role of PLZF in regulating ILC3 development and function remains unknown. Here, we show that PLZF was specifically expressed in mature intestinal ILC3s compared with other ILC subsets. PLZF was dispensable for ILC3 development. However, PLZF deficiency in ILC3s resulted in increased innate interleukin-22 (IL-22) secretion and protection against gut infection and inflammation. Mechanistically, PLZF negatively regulated IL-22 expression by ILC3s in a cell-intrinsic manner by binding to the IL-22 promoter region for transcriptional repression. Together, our data suggest that PLZF restricts intestinal ILC3 function to regulate gut immune homeostasis., (© 2023. The Author(s), under exclusive licence to CSI and USTC.)
- Published
- 2023
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