Tytgat Institute for Liver and Intestinal Research, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands.
Nat Immunol. 2013 Mar;14(3):221-9. doi: 10.1038/ni.2534. Epub 2013 Jan 20.
Innate lymphoid cells (ILCs) are effectors of innate immunity and regulators of tissue modeling. Recently identified ILC populations have a cytokine expression pattern that resembles that of the helper T cell subsets T(H)2, T(H)17 and T(H)22. Here we describe a distinct ILC subset similar to T(H)1 cells, which we call 'ILC1'. ILC1 cells expressed the transcription factor T-bet and responded to interleukin 12 (IL-12) by producing interferon-γ (IFN-γ). ILC1 cells were distinct from natural killer (NK) cells as they lacked perforin, granzyme B and the NK cell markers CD56, CD16 and CD94, and could develop from RORγt(+) ILC3 under the influence of IL-12. The frequency of the ILC1 subset was much higher in inflamed intestine of people with Crohn's disease, which indicated a role for these IFN-γ-producing ILC1 cells in the pathogenesis of gut mucosal inflammation.
先天淋巴细胞(ILC)是先天免疫的效应细胞和组织重塑的调节因子。最近鉴定的 ILC 群体具有类似于辅助性 T 细胞亚群 T(H)2、T(H)17 和 T(H)22 的细胞因子表达模式。在这里,我们描述了一种类似于 T(H)1 细胞的独特 ILC 亚群,我们称之为“ILC1”。ILC1 细胞表达转录因子 T-bet,并通过产生干扰素-γ(IFN-γ)对白细胞介素 12(IL-12)作出反应。ILC1 细胞与自然杀伤(NK)细胞不同,因为它们缺乏穿孔素、颗粒酶 B 和 NK 细胞标记物 CD56、CD16 和 CD94,并且可以在 IL-12 的影响下从 RORγt(+)ILC3 发育而来。在患有克罗恩病的人的炎症肠道中,ILC1 亚群的频率要高得多,这表明这些产生 IFN-γ 的 ILC1 细胞在肠道黏膜炎症的发病机制中起作用。