近日，日本筑波大学Akira Shibuya研究小组发现，1型先天淋巴样细胞（ILC1）通过干扰素-γ的分泌上调肝细胞中Bcl-xL表达来保护小鼠免受急性肝脏损伤。相关论文2019年12月3日在线发表在《免疫》上。

研究人员发现向小鼠注射四氯化碳（CCl4）激活了肝脏中的ILC1，但未激活自然杀伤（NK）细胞。激活的ILC1产生干扰素-γ（IFN-γ），并保护小鼠免受CCl4诱导的急性肝损伤。从激活的ILC1释放的IFN-γ通过Bcl-xL的上调促进了肝细胞的存活。肝ILC1的最佳活化和IFN-γ产生需要活化的NK受体DNAM-1。细胞外三磷酸腺苷可促进肝ILC1介导IL-12介导的IFN-γ产生。这些发现表明，ILC1对急性肝损伤期间的组织保护至关重要。

据了解，尽管最初发现ILC1作为肝脏驻留的ILC，但对其在肝脏中的病理生理作用的研究仍很少。

附：英文原文

Title: Type 1 Innate Lymphoid Cells Protect Mice from Acute Liver Injury via Interferon-γ Secretion for Upregulating Bcl-xL Expression in Hepatocytes

Author: Tsukasa Nabekura, Luke Riggan, Andrew D. Hildreth, Timothy E. O’Sullivan, Akira Shibuya

Issue&Volume: December 03, 2019

Abstract: Although type 1 innate lymphoid cells (ILC1s) have been originally found as liver-residentILCs, 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-γ (IFN-γ) and protected mice from CCl4-induced acute liver injury. IFN-γ released from activated ILC1s promoted the survivalof hepatocytes through upregulation of Bcl-xL. An activating NK receptor, DNAM-1,was required for the optimal activation and IFN-γ production of liver ILC1s. Extracellularadenosine triphosphate accelerated interleukin-12-driven IFN-γ production by liverILC1s. These findings suggest that ILC1s are critical for tissue protection duringacute liver injury.

DOI: 10.1016/j.immuni.2019.11.004

Source: https://www.cell.com/immunity/fulltext/S1074-7613(19)30462-5