Adipose-resident group 1 innate lymphoid cells promote obesity-associated insulin resistance
Open accessAbstract
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-γ 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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ILC1, ILC2, and ILC3 populations have been implicated in metabolic disorders beyond NAFLD, such as obesity.
“Of note, ILC1, ILC2 and ILC3 populations have been implicated in metabolic disorders beyond NAFLD (e.g. obesity).93,94”
From An integrated view of anti-inflammatory and antifibrotic targets for the treatment of NASH (2023) · cites this paper as [93]
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References 57 · Cited by 293
- Authors
- O’Sullivan, T. E., Rapp, M., Fan, X., Weizman, O.-E., Bhardwaj, P., Adams, N. M., Walzer, T., Dannenberg, A. J., & Sun, J. C.
- Affiliations
- Memorial Sloan Kettering Cancer Center (US)
- Cornell University (US)
- Centre International de Recherche en Infectiologie (FR)
- Corresponding author
- Sun, Joseph C.
- ORCID
- Venue
- Immunity
- Publisher
- Elsevier BV
- Published
- 2016-08
- Volume
- 45
- Issue
- 2
- Pages
- 428-441
- ISSN
- 1074-7613 (ISSN-L)
- PMC
- PMC5004886
- OpenAlex
- W2502313075
- Cited by
- 293
- References
- 57
- Citations by year
- 2026: 11 · 2025: 23 · 2024: 24 · 2023: 24 · 2022: 30 · 2021: 36 · 2020: 49 · 2019: 35 · 2018: 32 · 2017: 28 · 2016: 1
- FWCI
- 19.41
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Immunity (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- HAL (submittedVersion)
- Funders
- American Cancer Society
- Memorial Sloan-Kettering Cancer Center
- National Institutes of Health
- Weill Cornell Medical College
- Ludwig Center at Harvard
- National Cancer Institute (R01CA154481, P30CA008748)
- National Institute of General Medical Sciences (T32GM007739)
- National Institute of Allergy and Infectious Diseases (F30AI122721, R01AI100874)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › IL-33, ST2, and ILC Pathways
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
- Keywords
- ILC1, adipose tissue, obesity, insulin resistance, diet-induced obesity, IL-12, IL-12 receptor, STAT4, interferon-gamma, macrophage polarization, proinflammation, NFIL3, T-bet, natural killer cells, tissue residency
- MeSH terms
- T-bet Transcription Factor, Adipose Tissue, Animals, Cell Differentiation, Cells, Cultured, Humans, Immunity, Innate, Insulin Resistance, Interferon-gamma, Lymphocytes, Macrophages, Mice, Inbred C57BL, Mice, Transgenic, Obesity, Cytokines, Interleukin-12, Inflammation Mediators, T-Box Domain Proteins, STAT4 Transcription Factor, Basic-Leucine Zipper Transcription Factors, Mice
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