title: Autoantibodies and decreased expression of the transcription factor ELF-3 together with increased chemokine pathways support an autoimmune phenotype and altered differentiation in lichen planus located in oral mucosa.
abstract: BACKGROUND
  The pathogenesis of oral lichen planus (OLP), a chronic inflammatory disease, is not fully understood. It is known that OLP has autoimmune features, and it is suggested to be an autoimmune disease. ELF-3 is involved in differentiation of keratinocytes and deregulated in different tumours and inflammatory diseases. CXCR-3 and its ligands CXCL-10 and CXCL-11 are increased in autoimmune diseases and linked to Th-1 immune response.
  
  
  OBJECTIVE
  To analyse and compare expression of ELF-3, CXCR-3, CXCL-10 and CXCL-11 in OLP lesions and controls in whole and microdissected epithelium.
  
  
  METHODS
  Tissue biopsies from 20 patients clinically and histologically diagnosed with OLP and 20 healthy controls were studied using whole tissues or microdissected epithelium. By the use of qRT-PCR, mRNA levels of ELF-3, CXCR-3, CXCL-10 and CXCL-11 were studied. Western blot was used for analysis of ELF-3 protein expression. Sera from 19 OLP patients and 20 controls were analysed with ELISA in search for autoantibodies. Results  The upregulation of CXCR-3, CXCL-10 and CXCL-11 found in OLP is similar to previous findings showing an autoimmune phenotype in lichen planus (LP) and lichen sclerosus. Decreased expression of the differentiation-related transcription factor ELF-3 was also seen in OLP lesions, and we further demonstrate presence of circulating autoantibodies against the ELF-3 protein in sera from 3 of 19 (16%) LP patients tested.
  
  
  CONCLUSIONS
  On the basis of these findings, we confirm that OLP shows features of an autoimmune disease and suggest deregulated differentiation of keratinocytes to be one of the causes of the disease phenotype.
authors.affiliation: Department of Odontology, Umeå UniversityDepartment of Medical Biosciences, Umeå University, Umeå, SwedenTayside Tissue Bank/Medical Research Institute, University of Dundee, Ninewells Hospital and Medical School, Dundee, UKDepartment of Clinical Medicine and Public Health/Dermatology and Venerology, Umeå University, Umeå, Sweden.
authors.forename: K
authors.initials: K
authors.lastname: Danielsson
authors.forename: L
authors.initials: L
authors.lastname: Boldrup
authors.forename: M
authors.initials: M
authors.lastname: Rentoft
authors.forename: P J
authors.initials: PJ
authors.lastname: Coates
authors.forename: M
authors.initials: M
authors.lastname: Ebrahimi
authors.forename: E
authors.initials: E
authors.lastname: Nylander
authors.forename: Y B
authors.initials: YB
authors.lastname: Wahlin
authors.forename: K
authors.initials: K
authors.lastname: Nylander
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D001323:Autoantibodies / Q000378:metabolism*; D001483:Base Sequence; D015153:Blotting, Western; D018925:Chemokines / Q000378:metabolism*; D017931:DNA Primers; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D006801:Humans; D017676:Lichen Planus, Oral / Q000276:immunology* / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D010641:Phenotype; D016133:Polymerase Chain Reaction
chemical_list: D001323:Autoantibodies; D018925:Chemokines; D017931:DNA Primers