| First Author | Bando JK | Year | 2020 |
| Journal | J Exp Med | Volume | 217 |
| Issue | 2 | PubMed ID | 31699824 |
| Mgi Jnum | J:285055 | Mgi Id | MGI:6392708 |
| Doi | 10.1084/jem.20191520 | Citation | Bando JK, et al. (2020) ILC2s are the predominant source of intestinal ILC-derived IL-10. J Exp Med 217(2) |
| abstractText | 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. |
