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J Exp Med. 2019 Jun 27. pii: jem.20190689. doi: 10.1084/jem.20190689. [Epub ahead of print]

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

Author information

1
Medical Research Council Laboratory of Molecular Biology, Cambridge, UK.
2
Department of Respiratory, Inflammation and Autoimmunity, AstraZeneca, Cambridge, UK.
3
College of Medical and Dental Sciences, Institute of Immunology and Immunotherapy, University of Birmingham, Birmingham, UK.
4
Cardiovascular Medicine Division, Department of Medicine, University of Cambridge, Cambridge, UK.
5
Wellcome Trust Sanger Institute, Hinxton, UK.
6
Metabolic Research Laboratories, Addenbrooke's Treatment Centre, Institute of Metabolic Science, Addenbrooke's Hospital, University of Cambridge, Cambridge, UK.
7
Medical Research Council Laboratory of Molecular Biology, Cambridge, UK anm@mrc-lmb.cam.ac.uk.

Abstract

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.

PMID:
31248899
DOI:
10.1084/jem.20190689

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