Tissue microarray analysis of RANKL in cutaneous lupus erythematosus and psoriasis

Toberer, Ferdinand; Sykora, Jaromir; Göttel, Daniel; Ruland, Vincent; Hartschuh, Wolfgang; Enk, Alexander H.; Luger, Thomas A.; Beissert, Stefan; Loser, Karin; Joos, Stefan; Krammer, Peter H.; Kuhn, Annegret

doi:10.1111/j.1600-0625.2011.01303.x

Cited by 11 publications

(17 citation statements)

References 16 publications

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“…Notch gene expression has been reported in mouse and sheep skin during follicle initiation (8)(9)(10)(11). However, as Cre-mediated disruption of Notch signalling in fetal mouse epidermis did not inhibit follicle formation (10,12), its involvement, if any, must be through its action in the mesenchyme.…”

Section: Conflict Of Interestsmentioning

confidence: 99%

Apoptotic signal molecules in skin biopsies of cutaneous lupus erythematosus: analysis using tissue microarray

Toberer

Sykora

Göttel

et al. 2013

Experimental Dermatology

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Cutaneous lupus erythematosus (CLE) is a heterogeneous autoimmune disease. Different pathogenetic mechanisms, including the accumulation of apoptotic keratinocytes in CLE, have been reported. Therefore, we investigated whether CLE and other inflammatory skin diseases differ with regard to the epidermal expression of molecules that are crucial for the initiation and regulation of apoptosis. In this study, 241 skin biopsies from patients with CLE, psoriasis (PSO), lichen planus (LP) and healthy controls (HCs) were analysed immunohistochemically using the tissue microarray (TMA) technique. The TUNEL assay and anti-activated caspase-3 antibodies revealed a significant increase of apoptotic keratinocytes in CLE lesions compared with HCs. Furthermore, we detected a significant increase in the epidermal expression of CD95 in CLE specimens compared with PSO, LP and HCs. These data suggest that the accumulation of apoptotic keratinocytes in CLE might be due to the increased epidermal expression of CD95, resulting in increased activity of the extrinsic apoptotic pathway in the disease.

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Section: Conflict Of Interestsmentioning

confidence: 99%

Apoptotic signal molecules in skin biopsies of cutaneous lupus erythematosus: analysis using tissue microarray

Toberer

Sykora

Göttel

et al. 2013

Experimental Dermatology

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“…Background Environmental factors such as ultraviolet (UV) light have been identified to contribute to the activation of inflammatory and autoimmune diseases of the skin such as cutaneous lupus erythematosus (CLE) (1)(2)(3)(4)(5). UV irradiation induces various effects in the skin of CLE patients, such as cell death and inflammation (6)(7)(8), and several molecules, such as type I and III interferons (IFNs) and myxovirus protein A (MxA), an IFN-induced human protein expressed in CLE skin lesions, have been shown to be important biomarkers in the pathogenesis of the disease (9-13).…”

Section: Accepted For Publication 21 April 2014mentioning

confidence: 99%

Ultraviolet light protection by a sunscreen prevents interferon‐driven skin inflammation in cutaneous lupus erythematosus

Zahn

Graef

Patsinakidis

et al. 2014

Experimental Dermatology

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provided by future studies. For example, abnormal cytoplasmic Ca 2+ may be examined by mutagenesis and functional studies.Abnormal cytoplasmic Ca 2+ caused by haploinsufficiency of SPCA1 may alter post-translational modifications, including glycosylation, folding, trafficking and sorting, in cell adhesion molecules, leading to acantholytic changes seen in HHD (11-13). This study showed that different mutations in HHD result in distinct expression of mRNA and protein, which may relate to clinical phenotypes. AcknowledgementSee supporting information for details (Data S2). Author contributionMM, SN and KT performed the researches. HO and SI contributed samples. T. Hamada, CH and MF designed this study. MM and T. Hashimoto wrote the paper. Conflict of interestThe authors state no conflict of interest. Abstract: Irradiation with ultraviolet (UV) light is an important exacerbating factor in cutaneous lupus erythematosus (CLE) and induces various effects in the skin of patients with the disease, such as cell death and inflammation. Recently, we demonstrated the ability of a broad-spectrum sunscreen to prevent UV-induced damage both in patients with CLE and healthy controls (HCs). The aim of this study was to evaluate whether the UV-dependent activation of interferon (IFN)-driven inflammation in CLE can also be prevented by application of the sunscreen. In 20 patients with different subtypes of CLE and 10 HCs, defined areas on the upper back were treated with a broad-spectrum liposomal sunscreen 20 min prior to a combined standardized UVA/UVB irradiation. Immunohistological analyses using antibodies directed against MxA, CD11c, CD123 and CD68 were performed from skin biopsies taken from areas before UV irradiation as well as from sunscreen-treated and sunscreen-untreated areas 24 and 72 h after UV irradiation. The expression of MxA was completely prevented by the sunscreen applied prior to UV irradiation in CLE patients and HCs. Additionally, sunscreen protection significantly diminished the number of the CD11c-and CD123-positive dendritic cells, which are suggested to be a major source of type I/III IFNs, in UV-irradiated skin of patients with CLE. Moreover, the application of the sunscreen prevented the increase in CD68-positive macrophages in both groups 72 h after UV irradiation. The data of this study demonstrate that UV protection reduces lesional tissue damage and inhibits the typical IFN-driven inflammatory response in CLE.

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“…Toberer et al [12] found a significantly increased RANKL expression in psoriatic epidermis, while it was not observed in the patients with cutaneous lupus erythematosus. This could be explained by Treg functional insufficiency in psoriatic skin lesions that resulted in decreased effector T cell inhibition.…”

Section: Discussionmentioning

confidence: 99%

“…It has been shown that RANKL plays a significant role in regulation of numerous functions of the dendritic cells (DCs), such as enhancement of T cell activation capacity, increased release of proinflammatory cytokines, and prolonged cell survival. Moreover, RANKL is expressed on inflamed or activated keratinocytes and it induces activation of epidermal Langerhans cells (LCs) [12]. …”

Section: Introductionmentioning

confidence: 99%

The Assessment of Selected Bone and Cartilage Biomarkers in Psoriatic Patients from Poland

Bartosińska

Michalak-Stoma

Juszkiewicz-Borowiec

et al. 2015

Mediators of Inflammation

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Background. Psoriasis is an inflammatory disease in which joints involvement may be insidious and difficult to detect. Bone and cartilage biomarkers may be helpful in screening patients with psoriasis for psoriatic arthritis (PsA). Objectives. To assess bone and cartilage serum biomarkers in psoriasis. Methods. The study was conducted in 2014 and included 61 psoriatic patients and 30 healthy individuals. In both groups, the serum concentrations of soluble receptor activator of nuclear factor-κB ligand (sRANKL), cartilage oligomeric matrix protein (COMP), osteoprotegerin (OPG), and interleukin-20 (IL-20) were examined. Severity of skin lesions was assessed by Psoriasis Area and Severity Index (PASI), body surface area (BSA), and Physician Global Assessment (PGA) scores. Results. The duration of psoriasis was from 1 year to 45 years. 22 patients suffered from concomitant PsA. The mean value of PASI was 23.1 ± 12.0 and BSA was 27.6 ± 20.6%. COMP, OPG, and IL-20 concentrations in psoriatic patients were significantly higher than in the control group. OPG/sRANKL ratio was significantly lower in PsA patients than in psoriatic patients without arthritis. Conclusions. Results of the conducted study suggest that COMP, OPG, IL-20, and OPG/sRANKL ratio may appear useful biomarkers of bone and cartilage involvement in psoriasis.

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Tissue microarray analysis of RANKL in cutaneous lupus erythematosus and psoriasis

Cited by 11 publications

References 16 publications

Apoptotic signal molecules in skin biopsies of cutaneous lupus erythematosus: analysis using tissue microarray

Apoptotic signal molecules in skin biopsies of cutaneous lupus erythematosus: analysis using tissue microarray

Ultraviolet light protection by a sunscreen prevents interferon‐driven skin inflammation in cutaneous lupus erythematosus

The Assessment of Selected Bone and Cartilage Biomarkers in Psoriatic Patients from Poland

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