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.
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| http://dx.doi.org/10.1111/jcmm.15703 | DOI Listing |
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Article Synopsis
- Glucocorticoids are standard treatments for sudden sensorineural hearing loss, but some patients do not respond well to them, leading researchers to explore tanshinone IIA (TA) as a potential solution.
- The study investigates how TA might overcome glucocorticoid resistance by examining its effects on key proteins involved in cell proliferation and apoptosis in lab-created models simulating hearing loss.
- Results show that combining TA with dexamethasone enhances cell growth and reduces cell death, likely due to increased expression of specific regulatory proteins, suggesting that TA could be a valuable addition to existing treatments for improving outcomes in resistant patients.
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