Abstract
Infection with Toxoplasma gondii (T. gondii) during the pregnant period and its potentially miserable outcomes for the fetus, newborn, and even adult offspring continuously occur worldwide. People acquire infection through the consumption of infected and undercooked meat or contaminated food or water. T. gondii infection in pregnant women primarily during the gestation causes microcephaly, mental and psychomotor retardation, or death. Abnormal pregnancy outcomes are mainly associated with regulatory T cell (Treg) dysfunction. Tregs, a special subpopulation of T cells, function as a vital regulator in maintaining immune homeostasis. Tregs exert a critical effect on forming and maintaining maternal-fetal tolerance and promoting fetal development during the pregnancy period. Forkhead box P3 (Foxp3), a significant functional factor of Tregs, determines the status of Tregs. In this review, we summarize the effects of T. gondii infection on host Tregs and its critical transcriptional factor, Foxp3.
Highlights
T. gondii is an obligate intracellular parasite with a complicated life cycle, belonging to apicomplexa
We review the role of Tregs and the underlying mechanism in T. gondii-induced adverse pregnancy outcomes
Tregs play an immunosuppressive role through cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) and PD-1 binding to the target cell surface [80, 81] as well as secreting cytokines IL-10 and transforming growth factor-β (TGF-β) [77, 82], which are important for protective tolerance induced by Tregs during the pregnancy
Summary
T. gondii is an obligate intracellular parasite with a complicated life cycle, belonging to apicomplexa. Previous research has shown that the decrease in the number and function of Tregs of pregnant mice results from T. gondii excreted-secreted antigens [14], which break immune tolerance of normal pregnancy and cause abortion during early pregnancy [15]. M2 macrophages, which are induced by Th2 cytokines like IL-4 and IL-13, are alternatively activated/regenerative type that exert an immunosuppressive function and promote immune tolerance and tissue remodeling at the maternal-fetal interface [21].
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