ILC2s are the predominant source of intestinal ILC-derived IL-10

Jennifer K. Bando, Susan Gilfillan, Blanda Di Luccia, José L. Fachi, José L. Fachi, Cristiane Sécca, Marina Cella, Marco Colonna

Research output: Contribution to journalArticlepeer-review

13 Scopus citations

Abstract

Although innate lymphoid cells (ILCs) functionally analogous to T helper type 1 (Th1), Th2, and Th17 cells are well characterized, an ILC subset strictly equivalent to IL-10-secreting regulatory T cells has only recently been proposed. Here, we report the absence of an intestinal regulatory ILC population distinct from group 1 ILCs (ILC1s), ILC2s, and ILC3s in (1) mice bred in our animal facility; (2) mice from The Jackson Laboratory, Taconic Biosciences, and Charles River Laboratories; and (3) mice subjected to intestinal inflammation. Instead, a low percentage of intestinal ILC2s produced IL-10 at steady state. A screen for putative IL-10 elicitors revealed that IL-2, IL-4, IL-27, IL-10, and neuromedin U (NMU) increased IL-10 production in activated intestinal ILC2s, while TL1A suppressed IL-10 production. Secreted IL-10 further induced IL-10 production in ILC2s through a positive feedback loop. In summary, ILC2s provide an inducible source of IL-10 in the gastrointestinal tract, whereas ILCregs are not a generalizable immune cell population in mice.

Original languageEnglish
JournalJournal of Experimental Medicine
Volume217
Issue number2
DOIs
StatePublished - Feb 3 2020

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