Department of Pathology &Immunology, Washington University School of Medicine, 509 S. Euclid Ave Box 8118, St Louis, Missouri 63110, USA.
Nat Commun. 2017 Mar 31;8:14601. doi: 10.1038/ncomms14601.
The signals that maintain tissue-resident innate lymphoid cells (ILC) in different microenvironments are incompletely understood. Here we show that IL-7 receptor (IL-7R) is not strictly required for the development of any ILC subset, as residual cells persist in the small intestinal lamina propria (siLP) of adult and neonatal Il7ra mice. Il7ra ILC2 primarily express an ST2 phenotype, but are not inflammatory ILC2. CCR6 ILC3, which express higher Bcl-2 than other ILC3, are the most abundant subset in Il7ra siLP. All ILC subsets are functionally competent in vitro, and are sufficient to provide enhanced protection to infection with C. rodentium. IL-15 equally sustains wild-type and Il7ra ILC survival in vitro and compensates for IL-7R deficiency, as residual ILCs are depleted in mice lacking both molecules. Collectively, these data demonstrate that siLP ILCs are not completely IL-7R dependent, but can persist partially through IL-15 signalling.
维持组织驻留固有淋巴细胞（ILC）在不同微环境中的信号机制尚未完全阐明。本研究表明，IL-7 受体（IL-7R）并非 ILC 发育所必需，因为在成年和新生 Il7ra 小鼠的小肠固有层（siLP）中仍存在残留细胞。Il7ra ILC2 主要表达 ST2 表型，但不是炎症性 ILC2。CCR6 ILC3 比其他 ILC3 表达更高的 Bcl-2，是 Il7ra siLP 中最丰富的亚群。所有 ILC 亚群在体外均具有功能活性，足以提供对 C. rodentium 感染的增强保护。IL-15 在体外同样维持野生型和 Il7ra ILC 的存活，并弥补了 IL-7R 缺陷，因为缺乏这两种分子的小鼠中残留的 ILC 被耗尽。综上所述，这些数据表明，siLP ILC 并非完全依赖于 IL-7R，而是部分通过 IL-15 信号维持。
