CXCR3 <-> ligand–mediated skin inflammation in cutaneous lichenoid graft-versus-host disease Joerg Wenzel, MD, Svenja Lucas, Sabine Zahn, PhD, Sandra.

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Presentation transcript:

CXCR3 <-> ligand–mediated skin inflammation in cutaneous lichenoid graft-versus-host disease Joerg Wenzel, MD, Svenja Lucas, Sabine Zahn, PhD, Sandra Mikus, Dieter Metze, MD, Sonja Ständer, MD, Esther von Stebut, MD, Uwe Hillen, MD, Thomas Bieber, MD, PhD, Thomas Tüting, MD Journal of the American Academy of Dermatology Volume 58, Issue 3, Pages 437-442 (March 2008) DOI: 10.1016/j.jaad.2007.10.647 Copyright © 2008 American Academy of Dermatology, Inc. Terms and Conditions

Fig 1 Characterization of the inflammatory infiltrate in graft-versus-host disease (GVHD) and lichen planus. The inflammatory infiltrate was characterized by immunohistochemistry using monoclonal antibodies against the leukocyte surface markers CD3, CD4, CD8, CD20, CD56, and CD68, the cytotoxic proteins granzyme B and Tia1, and the chemokine receptor CXCR3. The infiltrate in lichenoid GVHD was dominated by T lymphocytes. CD4+ cells were mainly found in the perivascular areas, while those lymphocytes that infiltrated the basal epidermis were almost CD8+ cells (arrows). This figure depicts representative micrographs of lichenoid GVHD and lichen planus. The LSAB2 system (DAKO, Hamburg, Germany) with fast red as chromogen was used for visualization. Cells were counted per high power field (×200). Mean numbers ± SEM are shown. Journal of the American Academy of Dermatology 2008 58, 437-442DOI: (10.1016/j.jaad.2007.10.647) Copyright © 2008 American Academy of Dermatology, Inc. Terms and Conditions

Fig 2 Expression of type I interferon–associated proteins in graft-versus-host disease and lichen planus. This figure depicts representative micrographs of the expression of the antiviral protein MxA, which is a specific type I interferon surrogate marker, and the chemokine ligands CXCL9 and CXCL10. The expression of these proteins was scored semiquanitatively. Statistical evaluation was done using SPSS version 14, using the nonparametric Mann–Whitney U test. P < .05 was considered significant (∗); P < .01 was considered highly significant (∗∗). Journal of the American Academy of Dermatology 2008 58, 437-442DOI: (10.1016/j.jaad.2007.10.647) Copyright © 2008 American Academy of Dermatology, Inc. Terms and Conditions

Fig 3 Interferon-α1 mRNA in situ hybridization in graft-versus-host disease. PIQOR cDNA fragments for interferon-α1 were used as the template for generation of digoxigenin-labeled hybridization. Visualization was performed using alkaline phosphatase-conjugated anti-dig fab fragments with BICP/NBT 1mM levamisol as chromogen. This figure depicts the findings of IFNα in situ hybridization in a patient suffering from lichenoid graft-versus-host disease compared to the sense control. Journal of the American Academy of Dermatology 2008 58, 437-442DOI: (10.1016/j.jaad.2007.10.647) Copyright © 2008 American Academy of Dermatology, Inc. Terms and Conditions