Journal
JOURNAL OF INVESTIGATIVE DERMATOLOGY
Volume 132, Issue 3, Pages 658-666Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/jid.2011.369
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Funding
- ZonMW
- Netherlands Organization for Health Research and Development (AGIKO)
- Netherlands Genomics Initiative of NWO
- Netherlands Organization for Scientific Research
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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 (IFN gamma, CXCR3, CXCL9, CXCL10, CXCL11, CCR5, CCL4, and CCL5) specific for a Th1 IFN gamma-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.
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