ArticlemBio2025
PCV2 infection induces the differentiation of Treg cells via the TGF-β/Smad3 pathway.
Article in mBio, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
5 citing papers in PubMed.
- Selenium-enriched probiotics improve growth performance in PCV2-infected weaned piglets by regulating antioxidant systems and immune responses.Veterinary research communications · 2026Article
- Glucan-Based Nanoparticles Empower Precision Cancer Immunotherapy: Design Strategies, Immune Reprogramming Mechanisms, and Clinical Translation Prospects.International journal of nanomedicine · 2026Review
- Research Progress of Molecular HDrug design, development and therapy · 2026Review
- A porcine circovirus type 2d-based virus-like particle subunit vaccine effectively protects pigs against homologous challenge.Frontiers in microbiology · 2026Article
- Assessment of a porcine circovirus type 2 vaccine prototype through anatomopathological analysis and its correlation with blood viral load.Frontiers in veterinary science · 2025Article
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
In recent years, porcine circovirus type 2 (PCV2) has become a significant pathogenic virus in the swine industry, causing huge economic losses globally. However, the impact of PCV2 on the differentiation of CD4 IMPORTANCE: Porcine circovirus type 2 (PCV2) infection can cause immunosuppression-related diseases in pigs. Currently, it is still recognized as an important infectious pathogen of the swine industry in the world. In this study, we discovered that PCV2 infection disrupted the Th1/Th2/Th17/Treg immune equilibrium, and the differentiation capacity of Treg cells increased significantly. Briefly, PCV2 infection promoted the secretion of cytokine TGF-β, recruited Smad3, and phosphorylated it. Subsequently, the phosphorylated Smad3 transmitted the signal from the cell membrane to the nucleus and bound to the enhancer of Foxp3, thereby enhancing the transcription level of Foxp3 and facilitating the differentiation of Treg cells. This study enriches the pathogenic mechanism of PCV2 persistent infection and provided a theoretical basis for the prevention and control of immunosuppressive diseases.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.