Funding sources This study was supported by grants from Lion′s Cancer Research Foundation, Umeå University, the Swedish Cancer Society Contract number 11 0651 and Västerbotten County Council.
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
Article first published online: 8 NOV 2012
© 2012 The Authors. Journal of the European Academy of Dermatology and Venereology © 2012 European Academy of Dermatology and Venereology
Journal of the European Academy of Dermatology and Venereology
Volume 27, Issue 11, pages 1410–1416, November 2013
How to Cite
Danielsson, K., Boldrup, L., Rentoft, M., Coates, P.J., Ebrahimi, M., Nylander, E., Wahlin, Y.B. and Nylander, K. (2013), 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. Journal of the European Academy of Dermatology and Venereology, 27: 1410–1416. doi: 10.1111/jdv.12027
Conflict of Interest The authors state no conflict of interest.
- Issue published online: 16 OCT 2013
- Article first published online: 8 NOV 2012
- Received: 27 June 2012; Accepted: 03 October 2012
- Lion′s Cancer Research Foundation
- Umeå University
- Swedish Cancer Society. Grant Number: 11 0651
- Västerbotten County Council
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.
Objectives 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.