Journal
IMMUNITY
Volume 45, Issue 2, Pages 428-441Publisher
CELL PRESS
DOI: 10.1016/j.immuni.2016.06.016
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Funding
- American Cancer Society
- DAAD (Germany)
- NIH Medical Scientist Training Program [T32GM07739]
- NIH [1R01CA154481-01A1, AI100874, P30CA008748]
- Breast Cancer Research Foundation
- Botwinick-Wolfensohn Foundation
- Ludwig Center for Cancer Immunotherapy
- Searle Scholars Program
- Cancer Research Institute
- Starr Cancer Consortium
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Innate lymphoid cells (ILCs) function to protect epithelial barriers against pathogens and maintain tissue homeostasis in both barrier and non-barrier tissues. Here, utilizing Eomes reporter mice, we identify a subset of adipose group 1 ILC (ILC1) and demonstrate a role for these cells in metabolic disease. Adipose ILC1s were dependent on the transcription factors Nfil3 and T-bet but phenotypically and functionally distinct from adipose mature natural killer (NK) and immature NK cells. Analysis of parabiotic mice revealed that adipose ILC1s maintained long-term tissue residency. Diet-induced obesity drove early production of interleukin (IL)-12 in adipose tissue depots and led to the selective proliferation and accumulation of adipose-resident ILC1s in a manner dependent on the IL-12 receptor and STAT4. ILC1-derived interferon-g was necessary and sufficient to drive proinflammatory macrophage polarization to promote obesity-associated insulin resistance. Thus, adipose-resident ILC1s contribute to obesity-related pathology in response to dysregulated local proinflammatory cytokine production.
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