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Vulvar lichen sclerosus and lichen planus are T-cell-mediated chronic skin disorders. Although autoimmunity has been suggested, the exact pathogenesis of these disorders is still unknown. Therefore, the aim of the current study was to investigate the molecular and immunological mechanisms critical to the pathogenesis of vulvar lichen sclerosus and lichen planus. By using gene expression profiling and real-time RT-PCR experiments, we demonstrated a significantly increased expression of the pro-inflammatory cytokines (IFNγ, CXCR3, CXCL9, CXCL10, CXCL11, CCR5, CCL4, and CCL5) specific for a Th1 IFNγ-induced immune response. In addition, BIC/microRNA-155 (miR-155)-a microRNA involved in regulation of the immune response-was significantly upregulated in lichen sclerosus and lichen planus (9.5- and 17.7-fold change, respectively). Immunohistochemistry showed a significant T-cell response, with pronounced dermal infiltrates of CD4(+), CD8(+), and FOXP3(+) cells. In conclusion, these data demonstrate an autoimmune phenotype in vulvar lichen sclerosus and lichen planus, characterized by increased levels of Th1-specific cytokines, a dense T-cell infiltrate, and enhanced BIC/miR-155 expression.Journal of Investigative Dermatology advance online publication, 24 November 2011; doi:10.1038/jid.2011.369.
Department of Obstetrics and Gynecology, Erasmus University Medical Center, Rotterdam, The Netherlands.
This article was published in the following journal.
Name: The Journal of investigative dermatology
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Atrophy and shriveling of the SKIN of the VULVA that is characterized by the whitish LICHEN SCLEROSUS appearance, inflammation, and PRURITUS.
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