| First Author | Kudo F | Year | 2016 |
| Journal | Immunology | Volume | 147 |
| Issue | 1 | Pages | 21-9 |
| PubMed ID | 26425820 | Mgi Jnum | J:247265 |
| Mgi Id | MGI:5922080 | Doi | 10.1111/imm.12537 |
| Citation | Kudo F, et al. (2016) Interferon-gamma constrains cytokine production of group 2 innate lymphoid cells. Immunology 147(1):21-9 |
| abstractText | Group 2 innate lymphoid cells (ILC2s) produce a significant amount of interleukin-5 (IL-5), which supports eosinophil responses in various tissues; they also produce IL-13, which induces mucus production and contributes to tissue repair or fibrosis. The ILC2s are activated by alarmins, such as IL-33 released from epithelia, macrophages and natural killer T (NKT) cells in response to infection and allergen exposure, leading to epithelial injury. We examined gene expression in lung ILC2s and found that ILC2s expressed Ifngr1, the receptor for interferon-gamma (IFN-gamma). Interferon-gamma severely inhibited IL-5 and IL-13 production by lung and kidney ILC2s. To evaluate the effects in vivo, we used alpha-galactosylceramide (alpha-GalCer) to induce NKT cells to produce IL-33 and IFN-gamma. Intraperitoneal injection of alpha-GalCer in mice induced NKT cell activation resulting in IL-5 and IL-13 production by ILC2s. Administration of anti-IFN-gamma together with alpha-GalCer significantly enhanced the production of IL-5 and IL-13 by ILC2s in lung and kidney. Conversely, cytokine production from ILC2s was markedly suppressed after injection of exogenous IL-33 in Il33(-/-) mice pre-treated with alpha-GalCer. Hence, IFN-gamma induced or already present in tissues can impact downstream pleiotropic functions mediated by ILC2s, such as inflammation and tissue repair. |
