Journal
IMMUNITY
Volume 46, Issue 2, Pages 273-286Publisher
CELL PRESS
DOI: 10.1016/j.immuni.2017.01.008
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Funding
- American Diabetes JF Development Award [116JDF061]
- BWH Evergreen Innovation Grant
- BADERC grant
- ERC Stg grant [679173]
- Wallonie Bruxelles International Award
- NIH [5RO1AI113046]
- HMS Center for Immune Imaging
- [PO1 AI112521]
- European Research Council (ERC) [679173] Funding Source: European Research Council (ERC)
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Adipose tissue has a dynamic immune system that adapts to changes in diet and maintains homeostatic tissue remodeling. Adipose type 1 innate lymphoid cells (AT1-ILCs) promote pro-inflammatory macrophages in obesity, but little is known about their functions at steady state. Here we found that human and murine adipose tissue harbor heterogeneous populations of AT1-ILCs. Experiments using parabiotic mice fed a high-fat diet (HFD) showed differential trafficking of AT1-ILCs, particularly in response to short-and long-term HFD and diet restriction. At steady state, AT1-ILCs displayed cytotoxic activity toward adipose tissue macrophages (ATMs). Depletion of AT1-ILCs and perforin deficiency resulted in alterations in the ratio of inflammatory to anti-inflammatory ATMs, and adoptive transfer of AT1-ILCs exacerbated metabolic disorder. Diet-induced obesity impaired AT1-ILC killing ability. Our findings reveal a role for AT1-ILCs in regulating ATM homeostasis through cytotoxicity and suggest that this function is relevant in both homeostasis and metabolic disease.
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