Adipose-resident group 1 innate lymphoid cells promote obesity-associated insulin resistance Journal Article

   

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.
Article Title:	Adipose-resident group 1 innate lymphoid cells promote obesity-associated insulin resistance
Abstract:	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. © 2016 Elsevier Inc.
Journal Title:	Immunity
Volume:	45
Issue:	2
ISSN:	1074-7613
Publisher:	Cell Press
Date Published:	2016-08-16
Start Page:	428
End Page:	441
Language:	English
DOI:	10.1016/j.immuni.2016.06.016
PROVIDER:	scopus
PUBMED:	27496734
PMCID:	PMC5004886
DOI/URL:	https://www.scopus.com/inward/record.uri?eid=2-s2.0-84997701962&doi=10.1016%2fj.immuni.2016.06.016&partnerID=40&md5=371a5f85e29ad6d571fccd1733acd0b4
Notes:	Article -- Export Date: 3 January 2017 -- Source: Scopus

https://synapse.mskcc.org/synapse/works/has_related_data_chk/102890