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Journal of the American Academy of Dermatology
Volume 58, n° 3
pages 437-442 (mars 2008)
Doi : 10.1016/j.jaad.2007.10.647

CXCR3 <-> ligand–mediated skin inflammation in cutaneous lichenoid graft-versus-host disease

Joerg Wenzel, MD a, , Svenja Lucas a, Sabine Zahn, PhD a, Sandra Mikus a, Dieter Metze, MD b, Sonja Ständer, MD b, Esther von Stebut, MD c, Uwe Hillen, MD d, Thomas Bieber, MD, PhD a, Thomas Tüting, MD a
a Department of Dermatology at the Universitie of Bonn, Bonn, Germany 
b Department of Dermatology at the University of Münster, Münster, Germany 
c Department of Dermatology at the University of Mainz, Mainz, Germany 
d Department of Dermatology at the University of Essen, Essen, Germany 

Correspondence to: Joerg Wenzel, MD, Department of Dermatology, University of Bonn, Sigmund-Freud-Strasse 25, 53105 Bonn.

Lichenoid graft-versus-host disease (liGVHD) histologically shares several common features with other lichenoid dermatoses, such as cutaneous lupus erythematosus and lichen planus (LP), which collectively show a junctional infiltrate of cytotoxic lymphocytes with liquefaction of the basal layer (“interface dermatitis”). Because recent studies have shown a role for type I interferon (IFN)–associated inflammation, including lymphocyte recruitment via CXCR3 <-> ligand interaction in cutaneous lupus erythematosus and LP, we hypothesized that similar mechanisms might also be involved in liGVHD.


Ten representative lesional skin biopsies taken from patients with different subsets of chronic cutaneous graft versus host disease (GvDH) were recovered from the authors’ archives. Eight LP specimens and 5 punch biopsies taken from healthy skin were analyzed for control purposes. Immunohistochemistry was performed to characterize the lesional infiltrate (CD3, CD4, CD8, CD20, CD56, or CD68), to analyze type I IFN signaling (MxA), and to investigate expression of the IFN-inducible chemokines CXCL9 and CXCL10 and their ligand CXCR3. In situ hybridization was performed to visualize IFN⍺ expression on the mRNA level.


Our analyses revealed striking similarities between the inflammatory pattern seen in LP and liGVHD. Both disorders presented with a predominantly T-cellular inflammation with CD8+ lymphocytes affecting the basal epidermal layer. The majority of lesional lymphocytes expressed the chemokine receptor CXCR3. The corresponding chemokines CXCL9 and CXCL10 were found in the epidermis and within the inflammatory infiltrate. Analyses of MxA and IFN⍺ mRNA expression supported a role for type I IFNs in these conditions.


This study was limited by the number of well characterized cases in our archives. In situ hybridization was realizable only in single cases.


Our results support the hypothesis that CXCR3 <-> ligand–mediated lymphocyte recruitment is involved in cutaneous liGVHD. The fact that CXCL10 was seen in precisely those areas with extensive liquefaction of the basal epidermis supports a role of this chemokine for the development of the typical histologic “interface” pattern.

The full text of this article is available in PDF format.

 Supported by a grant from Bonn Forschung (BONFOR), University of Bonn (to Drs Wenzel and Zahn).
 Conflicts of interest: None declared.
 Reprints not available from the authors.

© 2008  American Academy of Dermatology, Inc.@@#104156@@
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