Inflammation-related cytokines in oral lichen planus: an overview

J Oral Pathol Med. 2015 Jan;44(1):1-14. doi: 10.1111/jop.12142. Epub 2013 Dec 16.

Abstract

Cytokines are powerful mediators which play a central role in both innate and adapted immune responses. Aberrant productions of cytokines may lead to the onset of immune deficiency, allergy or autoimmunity, which are involved in the mechanisms of various immune-mediated inflammatory diseases. Oral lichen planus (OLP) is a chronic inflammation disease affecting the oral mucosa with unknown aetiology. Previous studies have described the abnormal expression patterns of various inflammation-related cytokines, such as IL-1, 2, 4, 5, 6, 8, 10, 12, 17, 18, TGF-β, IFN-γ and TNF-α, in lesions, saliva, serum and peripheral blood mononuclear cells from patients with OLP, which may reflect the immune dysregulation status and emerge as central players in the immunopathogenesis of OLP. Besides, the gene polymorphisms of several cytokines such as IFN-γ, TNF-α, IL-4, IL-10 have been found to be involved in the susceptibility of OLP. In this review, we gave a brief introduction of the characteristics and biological functions of these inflammation-related cytokines and summarized for the first time the current knowledge on the involvement of inflammation-related cytokines in OLP. Further research on the exact roles of these cytokines will aid the understanding of the pathogenesis and the identification of novel therapeutic approaches of OLP.

Keywords: cytokine; oral lichen planus; overview.

Publication types

  • Review

MeSH terms

  • Cytokines / analysis*
  • Cytokines / genetics
  • Genetic Predisposition to Disease / genetics
  • Humans
  • Inflammation Mediators / analysis*
  • Interferon-gamma / analysis
  • Interleukins / analysis
  • Lichen Planus, Oral / genetics
  • Lichen Planus, Oral / immunology*
  • Polymorphism, Genetic / genetics
  • Transforming Growth Factor beta / analysis
  • Tumor Necrosis Factor-alpha / analysis

Substances

  • Cytokines
  • Inflammation Mediators
  • Interleukins
  • Transforming Growth Factor beta
  • Tumor Necrosis Factor-alpha
  • Interferon-gamma