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J Exp Med. 2019 Sep 2;216(9):1999-2009. doi: 10.1084/jem.20190689. Epub 2019 Jun 27.

A stromal cell niche sustains ILC2-mediated type-2 conditioning in adipose tissue.

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Medical Research Council Laboratory of Molecular Biology, Cambridge, UK.
Department of Respiratory, Inflammation and Autoimmunity, AstraZeneca, Cambridge, UK.
College of Medical and Dental Sciences, Institute of Immunology and Immunotherapy, University of Birmingham, Birmingham, UK.
Cardiovascular Medicine Division, Department of Medicine, University of Cambridge, Cambridge, UK.
Wellcome Trust Sanger Institute, Hinxton, UK.
Metabolic Research Laboratories, Addenbrooke's Treatment Centre, Institute of Metabolic Science, Addenbrooke's Hospital, University of Cambridge, Cambridge, UK.
Medical Research Council Laboratory of Molecular Biology, Cambridge, UK


Group-2 innate lymphoid cells (ILC2), type-2 cytokines, and eosinophils have all been implicated in sustaining adipose tissue homeostasis. However, the interplay between the stroma and adipose-resident immune cells is less well understood. We identify that white adipose tissue-resident multipotent stromal cells (WAT-MSCs) can act as a reservoir for IL-33, especially after cell stress, but also provide additional signals for sustaining ILC2. Indeed, we demonstrate that WAT-MSCs also support ICAM-1-mediated proliferation and activation of LFA-1-expressing ILC2s. Consequently, ILC2-derived IL-4 and IL-13 feed back to induce eotaxin secretion from WAT-MSCs, supporting eosinophil recruitment. Thus, MSCs provide a niche for multifaceted dialogue with ILC2 to sustain a type-2 immune environment in WAT.

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