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

Division of Molecular and Experimental Surgery, University Medical Center Erlangen, Erlangen, Germany.
Experimental Dermatology (Impact Factor: 4.12). 02/2011; 20(2):102-6. DOI: 10.1111/j.1600-0625.2010.01160.x
Source: PubMed

ABSTRACT 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)-α and IFN-γ 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-α and -γ 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.

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Available from: Joerg Wenzel, Jul 28, 2015
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    • "In accord with the proposed mechanism, inhibitors of TLR7 and TLR9 signaling in a lupus-prone murine model of interface dermatitis attenuated the skin lesions [88]. Moreover, a recently identified IFNα-and γ-induced protein—the GTPase human guanylate binding protein- 1 (GBP-1)—is expressed by keratinocytes and endothelial cells in primary and ultraviolet-(UV-) induced skin lesions from patients with various subtypes of CLE compared to nonlesional skin [89]. It has also been recently demonstrated that the IFNα-inducible IFI16 protein—normally localized in the nucleus—translocates in the cytoplasm of affected skin cells from lupus patients and in UV irradiated keratinocytes—leading to generation of antibodies against the IFNα-inducible IFI16 recently detected in sera of lupus patients [90] "
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