Imbalance of uterine innate lymphoid cells is involved in the abnormal pregnancy induced by Toxoplasma gondii infection.

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.