Agradecimentos: We would like to thank Brian Edelson and Nicholas Jarjour for reagents (Washington University School of Medicine, St. Louis, MO). We would also like to thank Michael Patnode and Adelle McFarland for scientific discussion and for critical reading of the manuscript. These studies were supported by the National Institutes of Health grants AI095542, DE025884, and AI134236 (to M. Colonna); AI134035 (to M. Colonna); and K99 DK118110 (to J.K. Bando). M. Colonna received research support from Pfizer. The authors declare no competing financial interests. Author contributions:J.K. Bando, S. Gilfillan, M. Cella, and M. Colonna designed experiments. J.K. Bando, S. Gilfillan, B. DiLuccia, J.L. Fachi, and C. Sécca performed experiments. J.K. Bando analyzed data and wrote the paper Ver menos

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 Ver menos