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Role of the high mobility group box 1 signalling axes via the receptor for advanced glycation end‐products and toll‐like receptor‐4 in the immunopathology of oral lichen planus: a potential drug target?
Author(s) -
Salem Abdelhakim,
Almahmoudi Rabeia,
Vehviläinen Mari,
Salo Tuula
Publication year - 2018
Publication title -
european journal of oral sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.802
H-Index - 93
eISSN - 1600-0722
pISSN - 0909-8836
DOI - 10.1111/eos.12416
Subject(s) - rage (emotion) , immunostaining , receptor , proinflammatory cytokine , glycation , oral lichen planus , hmgb1 , toll like receptor , high mobility group , immunology , biology , medicine , chemistry , gene , immunohistochemistry , inflammation , innate immune system , biochemistry , neuroscience
High mobility group box 1 ( HMGB 1) is an extremely conserved DNA ‐binding protein that stabilizes nucleosomes and facilitates gene transcription in mammalian cells. When released extracellularly, HMGB 1 becomes an alarmin that can mediate systemic diseases. High mobility group box 1 signals via two main receptors: receptor for advanced glycation end‐products ( RAGE ) and toll‐like receptor‐4 ( TLR 4). We hypothesized that HMGB 1 expression is increased in patients with oral lichen planus ( OLP ) relative to healthy controls. Therefore, HMGB 1 and its receptors were mapped in tissue biopsies from 25 patients with OLP and from 20 healthy controls by immunostaining and ImageJ analysis. High mobility group box 1 was induced in oral keratinocytes in all patients with OLP . The band‐like cell infiltrate in patients with OLP revealed very strong staining for RAGE . Likewise, TLR 4 was overexpressed throughout OLP mucosa which co‐localized with HMGB 1. In conclusion, we suggest that OLP could partly be an HMGB 1‐mediated condition by creating a proinflammatory loop cycle via RAGE ‐ and TLR 4‐signalling axes, which may contribute to the chronicity of this disease.