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Sirtuin 6 maintains epithelial STAT6 activity to support intestinal tuft cell development and type 2 immunity
Xiwen Xiong1,2, Chenyan Yang3,4, Wei-Qi He5
1School of Forensic Medicine, Xinxiang Medical University, Xinxiang, Henan, 453003, China. xwxiong@xxmu.edu.cn.
Nature Communications
|September 3, 2022
Summary
SIRT6 protein is vital for intestinal health and immunity against parasitic worm infections. Its absence impairs cell development and immune responses, while its presence enhances healing and parasite clearance.
Area of Science:
- Immunology
- Cell Biology
- Gastroenterology
Background:
- Intestinal epithelial cell (IEC) differentiation is key for gut homeostasis and immunity.
- SIRT6, an NAD+-dependent deacetylase, has known roles in aging, metabolism, and disease.
Purpose of the Study:
- To investigate the role of SIRT6 in intestinal epithelial cell differentiation and immune responses during helminth infection.
- To elucidate the molecular mechanisms by which SIRT6 regulates these processes.
Main Methods:
- Generation and analysis of IEC-specific Sirt6 knockout and transgenic mice.
- Assessment of tuft cell development, type 2 immunity, and helminth expulsion.
- Molecular analysis of signaling pathways, including STAT6 phosphorylation and SOCS3 expression.
Main Results:
- IEC Sirt6 deletion impaired tuft cell development and type 2 immunity, hindering worm expulsion.
- IEC SIRT6 overexpression enhanced epithelial remodeling and worm clearance.
- Sirt6 ablation increased SOCS3 expression, reducing STAT6 phosphorylation in IECs.
- STAT6 activation in intestinal epithelium promoted tuft and goblet cell expansion and reversed Sirt6 ablation defects.
Conclusions:
- SIRT6 plays a critical role in regulating intestinal epithelial remodeling and mucosal type 2 immunity during helminth infection.
- SIRT6 influences tuft cell development and STAT6 signaling, impacting host defense against parasites.
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