| First Author | Nabekura T | Year | 2020 |
| Journal | Immunity | Volume | 52 |
| Issue | 1 | Pages | 96-108.e9 |
| PubMed ID | 31810881 | Mgi Jnum | J:288506 |
| Mgi Id | MGI:6432231 | Doi | 10.1016/j.immuni.2019.11.004 |
| Citation | Nabekura T, et al. (2020) Type 1 Innate Lymphoid Cells Protect Mice from Acute Liver Injury via Interferon-gamma Secretion for Upregulating Bcl-xL Expression in Hepatocytes. Immunity 52(1):96-108.e9 |
| abstractText | Although type 1 innate lymphoid cells (ILC1s) have been originally found as liver-resident ILCs, their pathophysiological role in the liver remains poorly investigated. Here, we demonstrated that carbon tetrachloride (CCl4) injection into mice activated ILC1s, but not natural killer (NK) cells, in the liver. Activated ILC1s produced interferon-gamma (IFN-gamma) and protected mice from CCl4-induced acute liver injury. IFN-gamma released from activated ILC1s promoted the survival of hepatocytes through upregulation of Bcl-xL. An activating NK receptor, DNAM-1, was required for the optimal activation and IFN-gamma production of liver ILC1s. Extracellular adenosine triphosphate accelerated interleukin-12-driven IFN-gamma production by liver ILC1s. These findings suggest that ILC1s are critical for tissue protection during acute liver injury. |
