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-γ (IFN-γ) and protected mice from CCl4-induced acute liver injury. IFN-γ 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-γ production of liver ILC1s. Extracellular adenosine triphosphate accelerated interleukin-12-driven IFN-γ production by liver ILC1s. These findings suggest that ILC1s are critical for tissue protection during acute liver injury.

中文翻译：

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1 型先天性淋巴细胞通过分泌干扰素-γ 上调肝细胞中 Bcl-xL 的表达来保护小鼠免受急性肝损伤。

尽管 1 型先天性淋巴样细胞 (ILC1) 最初是作为肝脏驻留的 ILC 被发现的，但它们在肝脏中的病理生理学作用仍缺乏研究。在这里，我们证明了向小鼠体内注射四氯化碳 (CCl4) 会激活肝脏中的 ILC1，但不会激活自然杀伤 (NK) 细胞。激活的 ILC1s 产生干扰素-γ (IFN-γ) 并保护小鼠免受 CCl4 诱导的急性肝损伤。活化的 ILC1 释放的 IFN-γ 通过上调 Bcl-xL 促进肝细胞的存活。激活 NK 受体 DNAM-1 是肝脏 ILC1 的最佳激活和 IFN-γ 产生所必需的。细胞外三磷酸腺苷加速肝脏 ILC1 产生白细胞介素 12 驱动的 IFN-γ。这些发现表明 ILC1 对急性肝损伤期间的组织保护至关重要。