Original Article

Subject Category: Immunology/Infection

Journal of Investigative Dermatology (2008) 128, 67–78; doi:10.1038/sj.jid.5700945; published online 16 August 2007

Gene Expression Profiling of Lichen Planus Reflects CXCL9+-Mediated Inflammation and Distinguishes this Disease from Atopic Dermatitis and Psoriasis

Joerg Wenzel1,5, Bettina Peters2,5, Sabine Zahn1, Michael Birth2, Kay Hofmann2, Daniel Küsters2, Stefan Tomiuk2, Jens M Baron3, Hans F Merk3, Cornelia Mauch4, Thomas Krieg4, Thomas Bieber1, Thomas Tüting1 and Andreas Bosio2

  1. 1Department of Dermatology, University of Bonn, Bonn, Germany
  2. 2Miltenyi Biotec GmbH, MACSmolecular Business Unit, Cologne, Germany
  3. 3Department of Dermatology and Allergology, University Hospital RWTH Aachen, Aachen, Germany
  4. 4Department of Dermatology and Venerology, University of Cologne, Cologne, Germany

Correspondence: Dr Joerg Wenzel, Department of Dermatology, University of Bonn, Sigmund-Freud-Strasse 25, Bonn 53105, Germany. E-mail: joerg.wenzel@ukb.uni-bonn.de

5These authors have contributed equally to this work.

Received 22 January 2007; Revised 13 March 2007; Accepted 29 March 2007; Published online 16 August 2007.

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Abstract

Here, we present data of a gene expression profiling approach to apply the diagnostic value and pathological significance of this method in different inflammatory skin diseases, using whole skin biopsies. Initially, SAGE™ was performed to identify frequent tags differentially expressed in various skin diseases. On the basis of these results, a new skin pathology-oriented PIQOR™ microarray was designed. Lichen planus (LP) was chosen as a model disease to evaluate this system. Controls included healthy skin, atopic dermatitis (AD), and psoriasis (Pso). Gene expression analyses using the topic-defined microarray followed by unclassified clustering was able to discriminate LP from AD and Pso. Genes significantly expressed in LP included type I IFN inducible genes and a specific chemokine expression pattern. The CXCR3 ligand, CXCL9, was the most significant marker for LP. In situ hybridization and immunohistochemistry confirmed the results and revealed that keratinocytes are type I IFN producers in LP skin lesions. Our results show that gene expression profiling using a skin-specific microarray is a reliable method to identify patients with LP in the chosen context and reflect recent models concerning the pathogenesis of this disease. Gene expression profiling might complement the diagnostic spectrum in dermatology and may provide new pathogenetic insights.

Abbreviations:

AD, atopic dermatitis; HC, healthy controls; IHC, immunohistochemistry; ISH, in situ hybridization; LP, lichen planus; MHC, major histocompatibility complex; Pso, psoriasis

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