Comprehensive Insight into Lichen Planus Immunopathogenesis

Abstract

Lichen planus is a chronic disease affecting the skin, appendages, and mucous membranes. A cutaneous lichen planus is a rare disease occurring in less than 1% of the general population, while oral illness is up to five times more prevalent; still, both forms equally impair the patient’s quality of life. The etiology of lichen planus is not entirely understood. Yet, immune-mediated mechanisms have been recognized since environmental factors such as hepatitis virus infection, mechanical trauma, psychological stress, or microbiome changes can trigger the disease in genetically susceptible individuals. According to current understanding, lichen planus immunopathogenesis is caused by cell-mediated cytotoxicity, particularly cytotoxic T lymphocytes, whose activity is further influenced by Th1 and IL-23/Th-17 axis. However, other immunocytes and inflammatory pathways complement these mechanisms. This paper presents a comprehensive insight into the actual knowledge about lichen planus, with the causal genetic and environmental factors being discussed, the immunopathogenesis described, and the principal effectors of its inflammatory circuits identified.

Lichen planus triggered by COVID-19 vaccination: A case series

“…These vaccines may consequently induce an increase in some skin conditions brought on by the aforementioned factors. [ 9 ] In addition to lichen planus, we may also see flare-ups of pemphigus, psoriasis, vitiligo, atopic dermatitis, neutrophilic dermatoses, acne vulgaris and certain connective tissue diseases. [ 10 ]…”

Senescence-associated secretory phenotypes in mesenchymal cells contribute to cytotoxic immune response in oral lichen planus

“…The role of NK cells in OLP pathogenesis remains unclear; however, previous studies have reported that NK cells constituted 2.3–15% of cellular infiltrates in cutaneous lichen planus [ 14 , 53 ]. Therefore, NK cells may provide an early stimulatory signal for the mobilization of CD4 + and CD8 + T cells upon their arrival in lichen planus-inflamed areas [ 54 ]. Our data from the bioinformatics analysis suggest the possibility of NK cell involvement in OLP pathogenesis, which may support the hypothesis mentioned above.…”

Correlations between schizophrenia and lichen planus: a two-sample bidirectional Mendelian randomization study

“…Mental stressors have the potential to induce atypical alterations in inflammatory factors, leading to immune dysfunction, which may contribute to the development of LP, as immune-mediated mechanisms of LP are well recognized ( 14 ). Some studies have also suggested that people with schizophrenia may have a higher risk of autoimmune diseases ( 15 ).…”