ArticleJournal of virology2005
Decreased migration of Langerhans precursor-like cells in response to human keratinocytes expressing human papillomavirus type 16 E6/E7 is related to reduced macrophage inflammatory protein-3alpha production.
Article in Journal of virology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
77 citing papers in PubMed, 141 citations in OpenAlex.
- Integrated Immune Escape in Cervical Cancer: HLA-I Dysfunction and Immune Checkpoint Signaling.International journal of molecular sciences · 2026Review
- Advances in immunotherapy for HPV-associated malignancies: emerging strategies and clinical progress.Frontiers in immunology · 2026Review
- Mathematical modelling of the role of Langerhans cells in the dynamics of HPV infection.Scientific reports · 2025Article
- Review
- The immune microenvironment of cancer of the uterine cervix.Histology and histopathology · 2024Review
- Unraveling Emerging Anal Cancer Clinical Biomarkers from Current Immuno-Oncogenomics Advances.Molecular diagnosis & therapy · 2024Review
- Epidemiology, Molecular Pathogenesis, Immuno-Pathogenesis, Immune Escape Mechanisms and Vaccine Evaluation for HPV-Associated Carcinogenesis.Pathogens (Basel, Switzerland) · 2023Review
- Review
- Carcinogenesis and management of human papillomavirus-associated cervical cancer.International journal of clinical oncology · 2023Review
- Tumor microenvironmental modification by the current target therapy for head and neck squamous cell carcinoma.Journal of experimental & clinical cancer research : CR · 2023Review
- Improving head and neck cancer therapies by immunomodulation of the tumour microenvironment.Nature reviews. Cancer · 2023Review
- Review
- Common Microbial Genital Infections and Their Impact on the Innate Immune Response to HPV in Cervical Cells.Pathogens (Basel, Switzerland) · 2022Article
- Oral Papillomatosis: Its Relation with Human Papilloma Virus Infection and Local Immunity-An Update.Medicina (Kaunas, Lithuania) · 2022Review
- Human papillomavirus and cervical cancer: an insight highlighting pathogenesis and targeting strategies.Virusdisease · 2022Review
- HPV and the Risk of HIV Acquisition in Women.Frontiers in cellular and infection microbiology · 2022Review
- The association of cervicovaginal Langerhans cells with clearance of human papillomavirus.Frontiers in immunology · 2022Review
- Chemoradiotherapy-induced increase in Th17 cell frequency in cervical cancer patients is associated with therapy resistance and early relapse.Molecular oncology · 2021Article
- HPV and Recurrent Respiratory Papillomatosis: A Brief Review.Life (Basel, Switzerland) · 2021Review
- Review
17 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Infection with high-risk human papillomavirus (HPV) types, particularly types 16 and 18, contributes to 90% of cervical cancer cases. HPV infects cutaneous or mucosal epithelium, tissue that is monitored for microbial infection or damage by Langerhans cells. In lesions produced by HPV type 16, there is a reduction in numbers of immune cells, especially Langerhans cells. Langerhans precursor cells selectively express CCR6, the receptor for macrophage inflammatory protein 3alpha (MIP-3alpha), and function as potent immune responders to inflamed epithelium and initiators of the innate immune response. It has been reported that E6 and E7 of high-risk HPVs interfere with immune mediators in order to suppress the recruitment of immune cells and antiviral activities of infected cells. Here we show that, following proinflammatory stimulus, HPV-16 E6 and E7 inhibit MIP-3alpha transcription, resulting in suppression of the migration of immature Langerhans precursor-like cells. Interestingly, the E6 and E7 proteins from the low-risk HPV types also inhibited MIP-3alpha transcription. These results suggest that one mechanism by which HPV-infected cells suppress the immune response may be through the inhibition of a vital alert signal, thus contributing to the persistence of HPV infection.
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What OpenQuestion holds
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.