ArticleParasites & vectors2022
Tim-3 downregulation by Toxoplasma gondii infection contributes to decidual dendritic cell dysfunction.
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 10 papers.
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Who cites it
10 citing papers in PubMed, 21 citations in OpenAlex.
- Toxoplasma gondii infection reduces CD59 expression through downregulation of JAK2/STAT3 signaling axis to enhance decidual NK cell cytotoxicity via the RAS/MAPK pathway.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Dysfunctional Decidual CD4Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Genetic polymorphisms of TIM-3 and its association with asthma in familial cluster asthma.Postepy dermatologii i alergologii · 2025Article
- Involvement of Tim-3 in Maternal-fetal Tolerance: A Review of Current Understanding.International journal of biological sciences · 2025Review
- Recurrent ocular toxoplasmosis is associated with interferon-gamma deficiency possibly due to genetic origin.BMJ open ophthalmology · 2024Article
- IL-27/Blimp-1 axis regulates the differentiation and function of Tim-3+ Tregs during early pregnancy.JCI insight · 2024Article
- The effect of Toxoplasma gondii infection on galectin-9 expression in decidual macrophages contributing to dysfunction of decidual NK cells during pregnancy.Parasites & vectors · 2024Article
- Glucocorticoids in lung cancer: Navigating the balance between immunosuppression and therapeutic efficacy.Heliyon · 2024Review
- Decidual natural killer cells dysfunction is caused by IDO downregulation in dMDSCs with Toxoplasma gondii infection.Communications biology · 2024Article
- LILRB4 regulates the function of decidual MDSCs via the SHP-2/STAT6 pathway during Toxoplasma gondii infection.Parasites & vectors · 2023Article
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundWomen in early pregnancy infected by Toxoplasma gondii may have severe adverse pregnancy outcomes, such as spontaneous abortion and fetal malformation. The inhibitory molecule T cell immunoglobulin and mucin domain 3 (Tim-3) is highly expressed on decidual dendritic cells (dDCs) and plays an important role in maintaining immune tolerance. However, whether T. gondii infection can cause dDC dysfunction by influencing the expression of Tim-3 and further participate in adverse pregnancy outcomes is still unclear.
methodsAn abnormal pregnancy model in Tim-3-deficient mice and primary human dDCs treated with Tim-3 neutralizing antibodies were used to examine the effect of Tim-3 expression on dDC dysfunction after T. gondii infection.
resultsFollowing T. gondii infection, the expression of Tim-3 on dDCs was downregulated, those of the pro-inflammatory functional molecules CD80, CD86, MHC-II, tumor necrosis factor-α (TNF-α), and interleukin-12 (IL-12) were increased, while those of the tolerant molecules indoleamine 2,3-dioxygenase (IDO) and interleukin-10 (IL-10) were significantly reduced. Tim-3 downregulation by T. gondii infection was closely associated with an increase in proinflammatory molecules and a decrease in tolerant molecules, which further resulted in dDC dysfunction. Moreover, the changes in Tim-3 induced by T. gondii infection further reduced the secretion of the cytokine IL-10 via the SRC-signal transducer and activator of transcription 3 (STAT3) pathway, which ultimately contributed to abnormal pregnancy outcomes.
conclusionsToxoplasma gondii infection can significantly downregulate the expression of Tim-3 and cause the aberrant expression of functional molecules in dDCs. This leads to dDC dysfunction, which can ultimately contribute to abnormal pregnancy outcomes. Further, the expression of the anti-inflammatory molecule IL-10 was significantly decreased by Tim-3 downregulation, which was mediated by the SRC-STAT3 signaling pathway in dDCs after T. gondii infection.
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