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.

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Toxoplasma gondii excreted‐secreted antigens (ESA) could result in adverse outcomes of pregnancy including abortion, stillbirth, foetal infection or teratogenesis in mice during early stage of pregnancy. Defective generation or function of regulatory T cells (Tregs) may account for those adverse pregnancy outcomes. Forkhead box p3 (Foxp3), which is the key transcriptional factor of Tregs, modulates its development and maintains inhibitory function. We previously demonstrated that ESA inhibited Foxp3 expression by attenuating transforming growth factor β RII/Smad2/Smad3/Smad4 pathway. In this study, we propose to study the role of ESA on the activity of Foxp3 promoter and explore potential mechanisms. We demonstrated that ESA suppressed Foxp3 promoter activity using dual‐luciferase reporter assay. ESA functioned at −443/−96 region of Foxp3 promoter to suppress its activity using truncated fragments of Foxp3 promoter. Further analysis revealed that suppressive role of ESA on Foxp3 promoter activity is related to specificity protein 1 (SP1). Transfection of expression plasmid of pcDNA3.1‐SP1 could restore the down‐regulation of Foxp3 induced by ESA. In conclusion, this study provides a new mechanism by which ESA could inhibit the Foxp3 promoter activity via SP1.

Background The HCC has seen a spike in the morbidity and the mortality rate in recent times. This calls for an urgent understanding of the underlying molecular mechanisms of the HCC and to speed up the quest for the search of the target molecules to ensure quick diagnosis and prognosis subsequently. TLCD1 is a gene only reported in membrane fluidity. The variations in the TLCD1 expression levels related to the infiltration of the immune cells in HCC and the prognosis shall be examined initially. Methods The data received from TCGA shall provide the details of the gene expression, clinicopathology analysis and immune infiltration, along with the enrichment analysis. Moreover, we also performed additional analysis of the bioinformatics available. The immune responses of TLCD1 expression in HCC were analyzed using CIBERSORT and TIMER, while the statistical analysis was handled through R. Results Higher TLCD1 expression is strongly correlated with a poor prognostic and worse overall survival. Specifically, the increase in TLCD1 expression positively correlated with Tregs cells and T cells CD4 memory resting. The pathways strongly associated with TLCD1 was fatty acid metabolism and PPAR signaling pathway. Conclusions From the outcome of the study, it could be surmised that TLCD1 could be considered as a potential target for future treatment of HCC, as it was observed to be associated with the tumor-infiltrating immune cells in tumor microenvironment, establishing itself as a novel potential prognostic biomarker in HCC.