ArticleMedical science monitor : international medical journal of experimental and clinical research2020
Immune Response of Plasmacytoid Dendritic Cells Stimulated by Human Papillomavirus (HPV) E6 in an In Vitro System.
Article in Medical science monitor : international medical journal of experimental and clinical research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
4 citing papers in PubMed, 4 citations in OpenAlex.
- Omics sciences for cervical cancer precision medicine from the perspective of the tumor immune microenvironment.Oncology research · 2025Review
- NK cells in HPV-related tumorigenesis: mechanisms and clinical applications.Frontiers in cellular and infection microbiology · 2025Review
- Plasmacytoid Dendritic Cells, the Expression of the Stimulator of Interferon Genes Protein (STING) and a Possible Role of Th17 Immune Response in Cervical Lesions Mediated by Human Papillomavirus.Indian journal of microbiology · 2023Article
- Human papillomavirus associated cervical lesion: pathogenesis and therapeutic interventions.MedComm · 2023Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND This study aimed to analyze the changes in plasmacytoid dendritic cell (pDC) immunophenotypes when co-cultured with Caski cells and stimulated by human papillomavirus (HPV) E6 in vitro, and thus to discuss the immunoregulatory roles of pDCs in the tumorigenesis of cervical cancer. MATERIAL AND METHODS The immunophenotypic expression of pDCs was analyzed under stimulation of HPV E6 and co-culturing with Caski cells in vitro. RESULTS HPV E6 infection caused significantly increased expression of CD40 in HPV16 M and HPV16 H groups MyD88 in HPV16 M,HPV16 H, and HPV18L groups; and TRAF6 in HPV16 M, HPV16 H, and HPV18L groups. pDCs co-cultured with Caski cells showed significantly lower expression of MyD88 and TRAF6 compared with the control. CONCLUSIONS The expression of MyD88 and TRAF6 might vary in different stages of HPV infection. pDCs might regulate CD40 to participate in the tumorigenesis and progression of cervical cancer, but related mechanisms still need further investigation.
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Registered trials
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