ArticlePloS one2017
TLR1-10, NF-κB and p53 expression is increased in oral lichenoid disease.
Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 21 citations in OpenAlex.
- TLR1-Regulated Ferroptosis Gene Decreases the Occurrence of Restless Legs Syndrome.Brain and behavior · 2025Article
- Article
- Probiotics as Potential Biological Immunomodulators in the Management of Oral Lichen Planus: What's New?International journal of molecular sciences · 2022Review
- TLR4 Expression in Ex-Lichenoid Lesions-Oral Squamous Cell Carcinomas and Its Surrounding Epithelium: The Role of Tumor Inflammatory Microenvironment.Biomolecules · 2022Article
- The Functional Mechanism of MicroRNA in Oral Lichen Planus.Journal of inflammation research · 2022Review
- Expression and Significance of TNF-α and NF-κB/p65 in Cutaneous Lichen Planus.Clinical, cosmetic and investigational dermatology · 2022Article
- Molecular docking analysis of syringic acid with proteins in inflammatory cascade.Bioinformation · 2022Article
- Omega-3 polyunsaturated fatty acids: a promising approach for the management of oral lichen planus.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2020Review
- Dietary Flavonoids in p53-Mediated Immune Dysfunctions Linking to Cancer Prevention.Biomedicines · 2020Review
- Human closed and open apex premolar teeth express different toll-like receptor.Molecular genetics & genomic medicine · 2020Article
- Study on the Role of Salivary Flora and NF-κB Inflammatory Signal Pathway in Oral Lichen Planus.Inflammation · 2020Article
- P53: A Guardian of Immunity Becomes Its Saboteur through Mutation.International journal of molecular sciences · 2020Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Toll-like receptors (TLRs) and nuclear factor-κB (NF-κB) in keratinocytes play an important role in dermatological autoimmune diseases. Tumour suppressor protein p53 regulates TLR expression. The aim of this study was to compare the expression of TLR1-TLR10, p53 and NF-κB in patients with oral lichenoid disease (OLD) with healthy mucosa. Oral mucosal biopsies from 24 patients with OLD and 26 healthy controls (HC) were analysed for the expression of TLR1-TLR10, NF-κB and p53 by immunohistochemistry. The expression of all TLRs was increased in OLD epithelia compared to HC samples and the difference was significant in TLR1, TLR3, TLR4, TLR5, TLR6 and TLR7. In the basement membrane zone, the immunoreactivity of TLR5 was significantly more intense in OLD compared to HC. In the intermediate layer, the immunoreactivity of NF-κB was significantly stronger in OLD, whereas the staining for p53 was more intense in all layers of OLD compared to HC samples. In OLD, a positive correlation between TLR2 and NF-κB in the basal layer and between TLR5, p53 and NF-κB in the intermediate layers was discovered. The expression of TLRs, p53 and NF-κB is increased in OLD, which may play a role in the pathogenesis of this chronic immune-mediated mucosal disease.
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