Toxoplasma gondii (T. gondii) is a ubiquitous intracellular protozoan parasite that causes adverse pregnancy outcomes. Innate lymphoid cells (ILCs) are critical mediators of mucosal immunity, and have been reported to play an important role in uterine vascular adaptation for successful pregnancy. However, the specific role of ILCs in T. gondii-infection-induced adverse pregnancy outcomes remains elusive. In the present study, we found that T. gondii infection caused the imbalance of uterine ILC cells (uILCs). It was characterized by substantially lower expression of the transcription factor GATA-3 and RORγt and higher expression of T-bet in uILCs. Consistent with the transcription factor changes, uILCs from T. gondii-infected mice produced much less IL-5 and IL-17 and substantially more IFN-γ and TNF-α than did uILCs from uninfected mice. Notably, IL-12, IL-18, and their receptors were increased in the uterus of T. gondii-infected mice. In vitro experiments showed that IL-12 and IL-18 treatment reduced the percentages of uILC2 and uILC3 and increased the percentages of uILC1. Conclusion, our data suggest that alterations in uILC composition may disrupt the balance of immune microenvironment after T. gondii infection and contribute to the adverse pregnancy outcomes caused by T. gondii infection.

弓形虫( T. gondii ) 是一种普遍存在的细胞内原生动物寄生虫，可导致不良妊娠结局。先天淋巴细胞 (ILC) 是粘膜免疫的关键介质，据报道，它在成功怀孕的子宫血管适应中发挥重要作用。然而，ILCs 在弓形虫感染引起的不良妊娠结局中的具体作用仍然难以捉摸。在本研究中，我们发现弓形虫感染导致子宫 ILC 细胞 (uILC) 的失衡。它的特点是转录因子 GATA-3 和 RORγt 的表达显着降低，而 T-bet 在 uILC 中的表达更高。与转录因子变化一致，来自弓形虫的uILC与未感染小鼠的 uILC 相比，感染小鼠产生的 IL-5 和 IL-17 少得多，而产生的 IFN-γ 和 TNF-α 明显增多。值得注意的是，IL-12、IL-18 及其受体在感染弓形虫的小鼠的子宫中增加。体外实验表明IL-12和IL-18处理降低了uILC2和uILC3的百分比并增加了uILC1的百分比。结论，我们的数据表明，uILC 组成的改变可能会破坏弓形虫感染后免疫微环境的平衡，并导致弓形虫感染引起的不良妊娠结局。