The immune system of human and mouse neonates is relatively immature. However, innate lymphoid cells (ILCs), commonly divided into the subsets ILC1, ILC2, and ILC3, are already present in the placenta and other fetal compartments and exhibit higher activity than what is seen in adulthood. Recent reports have suggested the potential role of ILCs, especially ILC2s, in spontaneous preterm labor, which is associated with brain damage and subsequent long-term neurodevelopmental deficits. Therefore, we hypothesized that ILCs, and especially ILC2s, play a role in preterm brain injury.

C57Bl/6J mice at postnatal day 6 were subjected to hypoxia-ischemia (HI) insult induced by left carotid artery ligation and subsequent exposure to 10% oxygen in nitrogen. The presence of ILCs and ILC2s in the brain was examined at different time points after HI. The contribution of ILC2s to HI-induced preterm brain damage was explored using a conditionally targeted ILC2-deficient mouse strain (Rorα^fl/flIL7r^Cre), and gray and white-matter injury were evaluated at 7 days post-HI. The inflammatory response in the injured brain was assessed using immunoassays and immunochemistry staining.

Significant increases in ILCs and ILC2s were observed at 24 h, 3 days, and 7 days post-HI in the injured brain hemisphere compared with the uninjured hemisphere in wild-type mice. ILC2s in the brain were predominantly located in the meninges of the injured ipsilateral hemispheres after HI but not in the brain parenchyma. Overall, we did not observe changes in cytokine/chemokine levels in the brains of Rorα^fl/flIL7r^Cre mice compared with wild type animals apart from IL-13. Gray and white-matter tissue loss in the brain was not affected after HI in Rorα^fl/flIL7r^Cre mice. Correspondingly, we did not find any differences in reactive microglia and astrocyte numbers in the brain in Rorα^fl/flIL7r^Cre mice compared with wild-type mice following HI insult.

After HI, ILCs and ILC2s accumulate in the injured brain hemisphere. However, ILC2s do not contribute to the development of brain damage in this mouse model of preterm brain injury.

人和小鼠新生儿的免疫系统相对不成熟。然而，通常分为 ILC1、ILC2 和 ILC3 亚群的先天性淋巴细胞 (ILC) 已经存在于胎盘和其他胎儿区室中，并且表现出比成年期更高的活性。最近的报告表明 ILC，尤其是 ILC2 在自发性早产中的潜在作用，这与脑损伤和随后的长期神经发育缺陷有关。因此，我们假设 ILC，尤其是 ILC2，在早产脑损伤中起作用。

C57Bl/6J 小鼠在出生后第 6 天受到左颈动脉结扎诱导的缺氧缺血 (HI) 损伤，随后暴露于 10% 氧气中的氮气。在 HI 后的不同时间点检查大脑中 ILC 和 ILC2 的存在。使用条件性靶向 ILC2 缺陷小鼠品系探索了 ILC2 对 HI 诱导的早产脑损伤的贡献。罗α^{佛罗里达州/佛罗里达州}IL7r^Cre)，灰质和白质损伤在 HI 后 7 天进行评估。使用免疫测定和免疫化学染色评估受伤大脑中的炎症反应。

在 HI 后 24 小时、3 天和 7 天，与野生型小鼠的未受伤半球相比，在受伤的大脑半球中观察到 ILC 和 ILC2 显着增加。大脑中的 ILC2 主要位于 HI 后受损同侧半球的脑膜中，但不在脑实质中。总的来说，我们没有观察到大脑中细胞因子/趋化因子水平的变化罗α^{佛罗里达州/佛罗里达州}IL7r^Cre将小鼠与除 IL-13 之外的野生型动物进行比较。在 HI 后，大脑中的灰质和白质组织损失不受影响罗α^{佛罗里达州/佛罗里达州}IL7r^Cre老鼠。相应地，我们没有发现大脑中反应性小胶质细胞和星形胶质细胞数量的任何差异。罗α^{佛罗里达州/佛罗里达州}IL7r^CreHI 损伤后的小鼠与野生型小鼠相比。

HI 后，ILCs 和 ILC2s 在受伤的大脑半球中积累。然而，ILC2 对这种早产脑损伤小鼠模型中脑损伤的发展没有贡献。