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

Research output: Contribution to journalArticlepeer-review


  • Batika M J Rana
  • Eric Jou
  • Jillian L Barlow
  • Noe Rodriguez-Rodriguez
  • Jennifer A Walker
  • Claire Knox
  • Helen E Jolin
  • Clare S Hardman
  • Meera Sivasubramaniam
  • Aydan Szeto
  • E Suzanne Cohen
  • Ian C Scott
  • Matthew A Sleeman
  • Chiamaka I Chidomere
  • Helle F Jorgensen
  • Stefania Carobbio
  • Antonio Vidal-Puig
  • Andrew N J McKenzie

Colleges, School and Institutes

External organisations

  • Medical Research Council Cancer Unit, Hutchison/Medical Research Council Research Centre, University of Cambridge, Cambridge, United Kingdom; European Molecular Biology Laboratory, European Bioinformatics Institute (EMBL-EBI), Hinxton, United Kingdom.
  • Department of Respiratory, Inflammation and Autoimmunity, AstraZeneca, Cambridge, UK.
  • Institute of Immunology & Immunotherapy; College of Medical and Dental Sciences; University of Birmingham; Birmingham UK
  • University of Manchester
  • 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 anm@mrc-lmb.cam.ac.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.

Bibliographic note

© 2019 Rana et al.


Original languageEnglish
Pages (from-to)1999-2009
Number of pages11
JournalThe Journal of Experimental Medicine
Issue number9
Early online date27 Jun 2019
Publication statusPublished - 2 Sep 2019

ASJC Scopus subject areas