A stromal cell niche sustains ILC2-mediated type-2 conditioning in adipose tissue
Research output: Contribution to journal › Article
Colleges, School and Institutes
- 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 firstname.lastname@example.org.
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.
|Number of pages||11|
|Journal||The Journal of Experimental Medicine|
|Early online date||27 Jun 2019|
|Publication status||Published - 2 Sep 2019|