A transitory, interleukin-25 (IL-25)-responsive, group 2 innate lymphoid cell (ILC2) subset induced during type 2 inflammation was recently identified as iILC2s. This study focuses on understanding the significance of this population in relation to tissue-resident nILC2s in the lung and intestine. RNA-sequencing and pathway analysis revealed the AP-1 superfamily transcription factor BATF (basic leucine zipper transcription factor, activating transcription factor-like) as a potential modulator of ILC2 cell fate. Infection of BATF-deficient mice with Nippostrongylus brasiliensis showed a selective defect in IL-25-mediated helminth clearance and a corresponding loss of iILC2s in the lung characterized as IL-17RBhigh, KLRG1high, BATFhigh, and Arg1low BATF deficiency selectively impaired iILC2s because it had no impact on tissue-resident nILC2 frequency or function. Pulmonary-associated iILC2s migrated to the lung after infection, where they represented an early source of IL-4 and IL-13. Although the composition of ILC2s in the small intestine was distinct from those in the lung, their frequency and IL-13 expression remained dependent on BATF, which was also required for optimal goblet and tuft cell hyperplasia. Findings support IL-25-responsive ILC2s as early sentinels of mucosal barrier integrity.

中文翻译：

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BATF 是 IL-25 反应性迁移性 ILC2 细胞命运和功能的重要调节剂。

在 2 型炎症期间诱导的暂时性白细胞介素 25 (IL-25) 响应性第 2 组先天性淋巴细胞 (ILC2) 亚群最近被鉴定为 iILC2。本研究的重点是了解这一人群与肺和肠中组织驻留 nILC2 相关的重要性。RNA 测序和通路分析揭示了 AP-1 超家族转录因子 BATF（碱性亮氨酸拉链转录因子，激活转录因子样）作为 ILC2 细胞命运的潜在调节剂。用巴西日圆线虫感染 BATF 缺陷小鼠显示出 IL-25 介导的蠕虫清除选择性缺陷和肺中 iILC2 的相应丢失，其特征为 IL-17RBhigh、KLRG1high、BATFhigh、和 Arg1low BATF 缺乏选择性地损害 iILC2，因为它对组织驻留的 nILC2 频率或功能没有影响。肺部相关的 iILC2 在感染后迁移到肺部，它们代表了 IL-4 和 IL-13 的早期来源。尽管小肠中 ILC2 的组成与肺中的不同，但它们的频率和 IL-13 表达仍然依赖于 BATF，这也是最佳杯状细胞和簇状细胞增生所必需的。研究结果支持 IL-25 反应性 ILC2 作为黏膜屏障完整性的早期哨兵。它们的频率和 IL-13 表达仍然依赖于 BATF，这也是最佳杯状细胞和簇状细胞增生所必需的。研究结果支持 IL-25 反应性 ILC2 作为黏膜屏障完整性的早期哨兵。它们的频率和 IL-13 表达仍然依赖于 BATF，这也是最佳杯状细胞和簇状细胞增生所必需的。研究结果支持 IL-25 反应性 ILC2 作为黏膜屏障完整性的早期哨兵。