title: Distinct interferon-gamma and interleukin-9 expression in cutaneous and oral lichen planus.
abstract: BACKGROUND
  Cutaneous (CLP) and oral lichen planus (OLP) as the main subtypes of lichen planus (LP) present with different clinical manifestation and disease course, although their histopathologic features such as the band-like lymphocyte infiltrate and keratinocyte apoptosis are similar. So far, the underlying cellular and molecular mechanisms remain poorly understood.
  
  
  OBJECTIVE
  The aim of this study was to characterize and compare the in situ cellular infiltrates, cytokine expression profiles and apoptosis markers in CLP and OLP.
  
  
  METHODS
  Using immunofluorescence staining and laser scanning microscopy, we evaluated the cellular infiltrate (CD1a, CD3, CD4, CD8, CD21, CD57, CD123), cytokine expression (interleukin (IL)-1, IL-6, IL-9, IL-10, IL-17, IL-22, IL-23, tumour necrosis factor-α, transforming growth factor-β, interferon (IFN)-γ), and apoptosis markers (Fas, Fas ligand, cleaved caspase-3, TUNEL) of 21 anonymized biopsy specimens of LP (11 CLP, 10 OLP).
  
  
  RESULTS
  Among infiltrating cells mainly T cells and natural killer (NK) cells as well as plasmacytoid dendritic cells (DC) were observed. A predominance of CD8+ T cells was noted in OLP. In both CLP and OLP, T helper (Th)1, Th9, Th17, and Th22-type cytokines were expressed. The expression of IL-9, IFN-γ and IL-22 was higher in CLP compared to that of OLP (P = 0.0165; P = 0.0016; P = 0.052 respectively). Expression of Fas and Fas ligand as well as cleaved caspase-3-positive cells was observed in the epithelium of all LP samples.
  
  
  CONCLUSIONS
  The cell and cytokine patterns of CLP and OLP were partially distinct and generally resembled those reported for autoimmune diseases. The presence of CD8+ and NK cells as well as Fas/Fas ligand expression suggested that various pathways involved in keratinocyte apoptosis are relevant for LP. These results might help to establish targeted therapies for LP.
authors.affiliation: Department of Dermatology, Inselspital, Bern University Hospital, University of Bern, Bern, Switzerland.
authors.forename: B
authors.initials: B
authors.lastname: Weber
authors.affiliation: Department of Dermatology, Inselspital, Bern University Hospital, University of Bern, Bern, Switzerland.
authors.forename: C
authors.initials: C
authors.lastname: Schlapbach
authors.affiliation: Institute of Pharmacology, University of Bern, Bern, Switzerland.
authors.forename: M
authors.initials: M
authors.lastname: Stuck
authors.affiliation: Institute of Pharmacology, University of Bern, Bern, Switzerland.
authors.forename: H-U
authors.initials: HU
authors.lastname: Simon
authors.affiliation: Department of Dermatology, Inselspital, Bern University Hospital, University of Bern, Bern, Switzerland.
authors.forename: L
authors.initials: L
authors.lastname: Borradori
authors.affiliation: Department of Dermatology, Inselspital, Bern University Hospital, University of Bern, Bern, Switzerland.
authors.forename: H
authors.initials: H
authors.lastname: Beltraminelli
authors.affiliation: Department of Dermatology, Inselspital, Bern University Hospital, University of Bern, Bern, Switzerland.
authors.forename: D
authors.initials: D
authors.lastname: Simon
mesh_terms: D017209:Apoptosis; D015415:Biomarkers; D015496:CD4-Positive T-Lymphocytes / Q000473:pathology; D006801:Humans; D007371:Interferon-gamma / Q000378:metabolism*; D016906:Interleukin-9 / Q000378:metabolism*; D008010:Lichen Planus / Q000378:metabolism* / Q000473:pathology; D017676:Lichen Planus, Oral / Q000378:metabolism* / Q000473:pathology; D012189:Retrospective Studies
chemical_list: D015415:Biomarkers; D016906:Interleukin-9; D007371:Interferon-gamma