Possible Role of EBV in the Pathogenesis of Oral Lichen Planus

Objective
Oral lichen planus (OLP) is considered a T cell-mediated chronic inflammatory
process activated by an unknown antigen, making basal keratinocytes vulnerable
to a cytotoxic cell mediated immune response. The aim is to summarize information on the role and pathways of Epstein–Barr virus (EBV) and immune cells in inducing OLP as an autoimmune lesion.
Methods
A search was conducted across databases of PubMed, Scopus, Research Gate,
Web of Science, Science Direct, and Google Scholar. A total of 127 studies were
identified that examined the potential correlation between EBV and oral epithelial
cells with OLP.
Results
We can assume that EBV can act both as an exogenous and an endogenous
antigen in the pathogenesis of OLP. An important role in detecting and capturing
antigens and modulating the adaptive immune response plays antigen-presenting
cells (APC), such as dendritic cells (Langerhans cells, LC). Although EBV shows
tropism for B cells and epithelial cells, under certain conditions it can infect monocytes, LCs, NK, and T lymphocytes. It means that under some circumstances of the chronic inflammatory process, EBV particles can react as endogenous agents. During the development of the autoimmune process, a decisive role is played by the loss of immune tolerance.
Conclusions
Factors like the activity of cytokines, chemokines, and autoantibodies secreted
by EBV-positive plasma cells, autoantigens formed due to virus protein mimicry of
human proteins, new self-peptides released from damaged tissues, self-reactive B
and T cells, dysregulation of LC function, the anti-apoptotic effect of EBV early lytic antigens, and an imbalance between inflammatory and anti-inflammatory immune cells facilitate the development of an autoimmune process.