ArticleParasites & vectors2025
ATF3-mediated inhibition of Trem2 by Toxoplasma gondii contributes to adverse pregnancy outcomes.
Article in Parasites & vectors, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed.
- Triggering receptor expressed on myeloid cell family in atherosclerosis: from mechanisms to intervention strategies.Cell communication and signaling : CCS · 2026Review
- Trem2 negatively regulates the MTOR-PKCα axis to protect againstFrontiers in cellular and infection microbiology · 2026Article
- Trem2-MICAL1-P-ERK Axis in Macrophages Confers Protection AgainstPathogens (Basel, Switzerland) · 2025Article
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Authors and funding
8 authors.
Funding
Abstract
backgroundApproximately one in three people worldwide have been exposed to Toxoplasma gondii (T. gondii). Primary infection with T. gondii during pregnancy can cause severe complications. Our previous study demonstrated that deficiency of triggering receptor expressed on myeloid cells 2 (Trem2) exacerbates pregnancy-related complications in T. gondii-infected mice. However, understanding the mechanisms by which T. gondii modulates Trem2 expression in macrophages remains an unmet challenge.
methodsA mouse pregnancy model of T. gondii infection and an in vitro cellular stimulation model using soluble T. gondii antigens (sTgAg) were used to assess Trem2 expression. Recombinant plasmids containing the full-length Trem2 promoter were constructed to evaluate the effect of sTgAg on promoter activity, followed by the construction of truncated promoter plasmids to identify key regulatory regions. Transcription factors potentially binding to the Trem2 promoter were predicted using PROMO and JASPAR, with ATF3 identified as responsive to sTgAg stimulation via western blot analysis. The binding of ATF3 to the Trem2 promoter was validated by chromatin immunoprecipitation (ChIP) assays. Finally, ATF3 knockdown experiments were performed to determine its role in mediating the inhibitory effect of sTgAg on Trem2 expression.
resultsT. gondii significantly suppressed Trem2 expression in both mouse placentas and cellular models, with truncated promoter assays identifying key regulatory regions of the Trem2 promoter inhibited by sTgAg. ATF3 was identified as a transcription factor responsive to sTgAg stimulation, which bound to the Trem2 promoter. Importantly, knockdown of ATF3 restored Trem2 expression, demonstrating its critical role in mediating the inhibitory effect of sTgAg.
conclusionsWe identified that sTgAg may target and inhibit Trem2 expression through the transcription factor ATF3, and inhibition of ATF3 activity may help maintain Trem2 expression in macrophages, providing a potential therapeutic approach to avert negative effects on pregnancy related to T. gondii infection.
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