Detection of myxovirus resistance protein A in lichen planus lesions and its relationship to hepatitis C virus

Summary Background  Lichen planus (LP) is an inflammatory disease of the skin and oral mucosa. Studies suggested that type I interferons (IFNs) could play an important role in the cytotoxic inflammation in LP. Type I IFNs stimulate the production of several IFN‐induced proteins including myxovirus r...

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Bibliographic Details
Published in:British journal of dermatology (1951) Vol. 160; no. 5; pp. 980 - 983
Main Authors: Shaker, O.G., Hantar, N., El-Tahlawi, S., El-Tawdi, A., El-Hadidi, H., Hantar, S., El-Refai, A., William, R.
Format: Journal Article
Language:English
Published: Oxford, UK Blackwell Publishing Ltd 01-05-2009
Wiley-Blackwell
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Summary:Summary Background  Lichen planus (LP) is an inflammatory disease of the skin and oral mucosa. Studies suggested that type I interferons (IFNs) could play an important role in the cytotoxic inflammation in LP. Type I IFNs stimulate the production of several IFN‐induced proteins including myxovirus resistance protein A (MxA protein). The association of LP and chronic hepatitis C is well established, with variable prevalence rates among different populations. Many authors have considered hepatitis C virus (HCV) as a possible antigen for inducing cytotoxic immune response in LP. Objectives  To investigate the role of type I IFNs in LP through the detection of MxA protein, and to compare the expression of MxA protein between HCV‐positive and HCV‐negative patients with LP in an attempt to clarify the role of HCV in the pathogenesis of LP. Methods  The study included 33 skin biopsies from patients with LP and 10 control biopsies. MxA mRNA was detected by reverse transcription‐polymerase chain reaction. HCV‐specific antibodies were detected in patient sera by enzyme‐linked immunosorbent assay. Results  Our analysis revealed a significantly higher level of MxA protein in all the LP skin biopsies compared with controls. The expression was significantly higher in HCV‐positive patients than in HCV‐negative patients. Conclusions  Type I IFNs play a role in the pathogenesis of LP, and HCV could induce LP through increasing the production of type I IFNs.
Bibliography:ArticleID:BJD9033
ark:/67375/WNG-L68ZGRLZ-Q
istex:BEB1BD46268E699E8E5B0CFDBAECB18CEDA50612
Conflicts of interest
None declared.
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ISSN:0007-0963
1365-2133
DOI:10.1111/j.1365-2133.2009.09033.x