| First Author | Molofsky AB | Year | 2015 |
| Journal | Immunity | Volume | 43 |
| Issue | 1 | Pages | 161-74 |
| PubMed ID | 26092469 | Mgi Jnum | J:258943 |
| Mgi Id | MGI:6142329 | Doi | 10.1016/j.immuni.2015.05.019 |
| Citation | Molofsky AB, et al. (2015) Interleukin-33 and Interferon-gamma Counter-Regulate Group 2 Innate Lymphoid Cell Activation during Immune Perturbation. Immunity 43(1):161-74 |
| abstractText | Group 2 innate lymphoid cells (ILC2s) and regulatory T (Treg) cells are systemically induced by helminth infection but also sustain metabolic homeostasis in adipose tissue and contribute to tissue repair during injury. Here we show that interleukin-33 (IL-33) mediates activation of ILC2s and Treg cells in resting adipose tissue, but also after helminth infection or treatment with IL-2. Unexpectedly, ILC2-intrinsic IL-33 activation was required for Treg cell accumulation in vivo and was independent of ILC2 type 2 cytokines but partially dependent on direct co-stimulatory interactions via ICOSL-ICOS. IFN-gamma inhibited ILC2 activation and Treg cell accumulation by IL-33 in infected tissue, as well as adipose tissue, where repression increased with aging and high-fat diet-induced obesity. IL-33 and ILC2s are central mediators of type 2 immune responses that promote tissue and metabolic homeostasis, and IFN-gamma suppresses this pathway, likely to promote inflammatory responses and divert metabolic resources necessary to protect the host. |
