TLR1-10, NF-kappa B and p53 expression is increased in oral lichenoid disease

Show full item record



Rusanen , P , Marttila , E , Uittamo , J , Hagström , J , Salo , T & Rautemaa-Richardson , R 2017 , ' TLR1-10, NF-kappa B and p53 expression is increased in oral lichenoid disease ' , PLoS One , vol. 12 , no. 7 , 0181361 .

Title: TLR1-10, NF-kappa B and p53 expression is increased in oral lichenoid disease
Author: Rusanen, Peter; Marttila, Emilia; Uittamo, Johanna; Hagström, Jaana; Salo, Tuula; Rautemaa-Richardson, Riina
Contributor organization: Clinicum
University of Helsinki
Department of Bacteriology and Immunology
Department of Oral and Maxillofacial Diseases
Department of Pathology
HUS Head and Neck Center
Date: 2017-07-17
Language: eng
Number of pages: 13
Belongs to series: PLoS One
ISSN: 1932-6203
Abstract: Toll-like receptors (TLRs) and nuclear factor-kappa B (NF-kappa B) 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-kappa B 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-kappa B 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-kappa B 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-kappa B in the basal layer and between TLR5, p53 and NF-kappa B in the intermediate layers was discovered. The expression of TLRs, p53 and NF-kappa B is increased in OLD, which may play a role in the pathogenesis of this chronic immune-mediated mucosal disease.
313 Dentistry
3111 Biomedicine
Peer reviewed: Yes
Rights: cc_by
Usage restriction: openAccess
Self-archived version: publishedVersion

Files in this item

Total number of downloads: Loading...

Files Size Format View
journal.pone.0181361.pdf 19.00Mb PDF View/Open

This item appears in the following Collection(s)

Show full item record