ArticlePloS one2018
Role of IL-23 signaling in the progression of premalignant oral lesions to cancer.
Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 19 citations in OpenAlex.
- The Role of IL-17 in the Pathogenesis of Oral Squamous Cell Carcinoma.International journal of molecular sciences · 2023Review
- Antibody-mediated blockade of the IL23 receptor destabilizes intratumoral regulatory T cells and enhances immunotherapy.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Periodontal Pathogens: A Crucial Link Between Periodontal Diseases and Oral Cancer.Frontiers in microbiology · 2022Review
- Innate lymphoid cells in early tumor development.Frontiers in immunology · 2022Review
- ADGRL4/ELTD1 Expression in Breast Cancer Cells Induces Vascular Normalization and Immune Suppression.Molecular cancer research : MCR · 2021Article
- Review
- IL-12 Family Cytokines in Cancer and Immunotherapy.Cancers · 2021Review
- Immunomodulation of T Helper Cells by Tumor Microenvironment in Oral Cancer Is Associated With CCR8 Expression and Rapid Membrane Vitamin D Signaling Pathway.Frontiers in immunology · 2021Article
- Possible Immunotherapeutic Strategies Based on Carcinogen-Dependent Subgroup Classification for Oral Cancer.Frontiers in molecular biosciences · 2021Review
- Microbial Colonization and Inflammation as Potential Contributors to the Lack of Therapeutic Success in Oral Squamous Cell Carcinoma.Frontiers in oral health · 2021Review
- Leukoplakia and Immunology: New Chemoprevention Landscapes?International journal of molecular sciences · 2020Review
- IL-23 and PSMA-targeted duo-CAR T cells in Prostate Cancer Eradication in a preclinical model.Journal of translational medicine · 2020Article
- Immune Suppression Mediated by STAT4 Deficiency Promotes Lymphatic Metastasis in HNSCC.Frontiers in immunology · 2019Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Mice bearing carcinogen-induced premalignant oral lesions were previously shown to have a pro-inflammatory phenotype, which is replaced with an immune inhibitory phenotype as lesions progress to cancer. Since Th17 cells are prominent at the premalignant lesion state and their levels are supported by IL-23, studies used mice that were IL-23 receptor deficient (IL-23R KO) to determine the requirement for IL-23 signaling in the immunological and clinical status of mice with premalignant oral lesions. The results showed a dependence on IL-23 signaling for the pro-inflammatory state of mice with oral lesions as levels of IL-2, IFN-γ, IL-6, IL-17 and TNF-α were elevated in wildtype mice with premalignant oral lesions, but not in IL-23R KO mice. In contrast, as lesions progressed to cancer, the pro-inflammatory phenotype subsided and was replaced with the inhibitory mediator IL-10 and with Treg cells in wildtype mice, although not in IL-23R KO mice. Clinically, early progression of premalignant oral lesions to cancer was enhanced in IL-23R KO mice compared to progression in wildtype mice. These results show the importance of IL-23 signaling in both the pro-inflammatory phenotype characteristic of premalignant oral lesions and the inhibitory phenotype as lesions progress to cancer.
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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.