Increased expression of guanylate binding protein-1 in lesional skin of patients with cutaneous lupus erythematosus

被引:23
作者
Naschberger, Elisabeth [1 ]
Wenzel, Joerg [2 ]
Kretz, Cosima C. [3 ]
Herrmann, Martin [4 ]
Stuerzl, Michael [1 ]
Kuhn, Annegret [3 ,5 ]
机构
[1] Univ Med Ctr Erlangen, Div Mol & Expt Surg, D-91054 Erlangen, Germany
[2] Univ Bonn, Dept Dermatol, D-5300 Bonn, Germany
[3] German Canc Res Ctr, Tumor Immunol Program, Div Immunogenet, D-6900 Heidelberg, Germany
[4] Univ Med Ctr Erlangen, Dept Internal Med 3, Inst Clin Immunol, D-91054 Erlangen, Germany
[5] Univ Munster, Dept Dermatol, Munster, Germany
关键词
guanylate binding protein; inflammation; interferon; lupus erythematosus; skin; UV light; PLASMACYTOID DENDRITIC CELLS; ENDOTHELIAL-CELLS; INFLAMMATORY CYTOKINES; ATOPIC-DERMATITIS; INTERFERON; INHIBITION; ACTIVATION; INDUCTION; GTPASE; CHEMOKINE;
D O I
10.1111/j.1600-0625.2010.01160.x
中图分类号
R75 [皮肤病学与性病学];
学科分类号
100206 ;
摘要
The large GTPase human guanylate binding protein-1 (GBP-1) is a key mediator of angiostatic effects of inflammation and is induced by interferon (IFN)-alpha and IFN-gamma in endothelial cells (ECs). The aim of this study was to investigate whether GBP-1 is a marker of skin lesions in patients with cutaneous lupus erythematosus (CLE). Western blotting revealed that GBP-1 was in vitro induced by IFN-alpha and -gamma in primary keratinocytes obtained from healthy controls. Moreover, we found that this protein was expressed by keratinocytes and ECs in primary and ultraviolet (UV)-induced skin lesions from patients with various subtypes of CLE, when compared to non-lesional skin. No GBP-1 expression was noted in skin biopsy specimens 24 or 72 h after UV irradiation prior to lesion formation in patients with CLE or in healthy control specimens with or without UV irradiation. Initial findings suggest that GBP-1 is not expressed in other skin diseases with different inflammatory aetiology, such as atopic dermatitis. We conclude that GBP-1 expression is closely associated with skin lesions in patients with CLE, suggesting a contribution of GBP-1 in the pathogenesis of this disease.
引用
收藏
页码:102 / 106
页数:5
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