TLR4 and TLR9 are induced in oral lichen planus.

Authors: Siponen, M  Kauppila, JH  Soini, Y  Salo, T 
Citation: Siponen M, etal., J Oral Pathol Med. 2012 Nov;41(10):741-7. doi: 10.1111/j.1600-0714.2012.01169.x. Epub 2012 Jun 5.
Pubmed: (View Article at PubMed) PMID:22672741
DOI: Full-text: DOI:10.1111/j.1600-0714.2012.01169.x

BACKGROUND: The role of Toll-like receptors (TLRs) has been elucidated in many human infectious, autoimmune and neoplastic diseases. Previously, TLR2 and TLR4 expression in oral lichen planus (OLP) was described. The aim of our study was to examine expression patterns of TLR4 and TLR9 in normal oral mucosa and OLP and describe the effect of topical tacrolimus treatment on the expression of TLR4 and TLR9 in OLP. METHODS: Toll-like receptor 4 and TLR9 expression was analysed by immunohistochemistry in five samples of normal oral mucosa and 50 samples of OLP (31 representing clinically white and 19 clinically erythematous/erosive lesions). We evaluated also the effect of topical tacrolimus on TLR4 and TLR9 expression in a patient with OLP. RESULTS: Toll-like receptor 4 and TLR9 expression was increased in OLP epithelium compared with normal epithelium (P < 0.001); no significant difference between the two clinical types of OLP was observed. TLR9 expression was strongest in the superficial layer of the epithelium (P < 0.001), while the expression of TLR4 was strongest in the basal layer (P < 0.001). Treatment of OLP lesions with topical tacrolimus resulted in clinical improvement but had no effect on TLR expression levels. CONCLUSIONS: Toll-like receptor 4 and TLR9 are induced in OLP; our finding confirms the results of a previous study. TLR4 and TLR9 may play a part in the pathogenesis of OLP. Further studies are needed to dissect the definitive role of TLRs in OLP pathogenesis and progression and to determine the effect of tacrolimus on the function of TLRs.


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CRRD ID: 7777153
Created: 2014-01-06
Species: All species
Last Modified: 2014-01-06
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.