A stromal cell niche sustains ILC2-mediated type-2 conditioning in adipose tissue.
Rana BMJ., Jou E., Barlow JL., Rodriguez-Rodriguez N., Walker JA., Knox C., Jolin HE., Hardman CS., Sivasubramaniam M., Szeto A., Cohen ES., Scott IC., Sleeman MA., Chidomere CI., Cruz Migoni S., Caamano J., Jorgensen HF., Carobbio S., Vidal-Puig A., McKenzie ANJ.
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.