Journal
CELL REPORTS
Volume 25, Issue 8, Pages 2053-+Publisher
CELL PRESS
DOI: 10.1016/j.celrep.2018.10.091
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Funding
- Belgian Program in Interuniversity Poles of Attraction
- Fonds Jean Brachet
- European Regional Development Fund [ERDF-Wallonia BioMed 2014-2020-LIV 45-20]
- Wallonia (Programme d'Excellence Food4Gut)
- National Fund for Scientific Research
- Belgian State
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Recent observations clearly highlight the critical role of type 2 innate lymphoid cells in maintaining the homeostasis of adipose tissues in humans and mice. This cell population promotes beiging and limits adiposity directly and indirectly by sustaining a Th2-prone environment enriched in eosinophils and alternatively activated macrophages. Accordingly, the number and function of type 2 innate lymphoid cells (ILC2s) are strongly impaired in obese individuals. In this work, we identify the PD-1-PD-L1 pathway as a factor leading to ILC2 destabilization upon high-fat feeding resulting in impaired tissue metabolism. Tumor necrosis factor (TNF) appears to play a central role, triggering interleukin-33 (IL-33)-dependent PD-1 expression on ILC2s and recruiting and activating PD-L1(hi) M1 macrophages. PD-1 blockade partially restores the type 2 innate axis, raising the possibility of restoring tissue homeostasis.
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