ArticleParasites & vectors2022
B7-H4 reduction induced by Toxoplasma gondii infection results in dysfunction of decidual dendritic cells by regulating the JAK2/STAT3 pathway.
Article in Parasites & vectors, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 36 citations in OpenAlex.
- The absence of B7-H4 inhibits PD-L1 expression by driving a methylation of PD-L1 promoter in breast cancer cells.Breast cancer research : BCR · 2026Article
- Membrane and soluble VTCN1 (B7H4) converge on Src signaling to mediate gemcitabine resistance in intrahepatic cholangiocarcinoma.Theranostics · 2026Article
- Harnessing 2D and 3D human endometrial cell culture models to investigate SARS-CoV-2 infection in early pregnancy.Clinical science (London, England : 1979) · 2025Article
- Article
- Decidual natural killer cells dysfunction is caused by IDO downregulation in dMDSCs with Toxoplasma gondii infection.Communications biology · 2024Article
- Single-cell transcriptomic analysis of decidual immune cell landscape in the occurrence of adverse pregnancy outcomes induced by Toxoplasma gondii infection.Parasites & vectors · 2024Article
- LILRB4 regulates the function of decidual MDSCs via the SHP-2/STAT6 pathway during Toxoplasma gondii infection.Parasites & vectors · 2023Article
- Tim-3 regulates the immunosuppressive function of decidual MDSCs via the Fyn-STAT3-C/EBPβ pathway during Toxoplasma gondii infection.PLoS pathogens · 2023Article
- Modeling the human placental barrier to understandFrontiers in cellular and infection microbiology · 2023Review
- Effect of B7-H4 downregulation induced by Toxoplasma gondii infection on dysfunction of decidual macrophages contributes to adverse pregnancy outcomes.Parasites & vectors · 2022Article
- Tim-3 downregulation by Toxoplasma gondii infection contributes to decidual dendritic cell dysfunction.Parasites & vectors · 2022Article
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundPrimary infection of Toxoplasma gondii can cause serious abnormal pregnancy outcomes such as miscarriage and stillbirth. Inhibitory molecule B7-H4 is abundantly expressed in dendritic cells (DCs) and plays an important role in maintaining immune tolerance. However, the role of B7-H4 in decidual DCs (dDCs) in T. gondii-induced abnormal pregnancy outcomes is not clear.
methodsWe established T. gondii-infected abnormal pregnancy model in wild-type (WT) and B7-H4 knockout (B7-H4
resultsOur results showed that T. gondii infection significantly decreased B7-H4 expression in dDCs. In addition, B7-H4
conclusionsTaken together, the results show that reduction of B7-H4 by T. gondii infection significantly modulates the decrease in cytokine IL-10 and enzyme IDO and the increase in cytokine IL-12, contributing to dDC dysfunction. Moreover, the JAK2/STAT3 pathway is involved in the regulation of B7-H4 by T. gondii infection and in the subsequent IDO and cytokine production, which ultimately contributes to abnormal pregnancy outcomes.
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