The safety and efficacy of light emitting diodes-based ultraviolet A1 phototherapy in bleomycin-induced scleroderma in mice

Karpec, Diana; Rudys, Romualdas; Leonavičienė, Laima; Mackiewicz, Z; Bradūnaitė, Rūta; Kirdaitė, Gailutė; Venalis, Algirdas

doi:10.1016/j.advms.2017.09.001

Cited by 7 publications

(5 citation statements)

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“…Furthermore, a recent report using transgenic mice that develop spontaneous skin fibrosis showed a major role for mast cells specifically in inducing inflammation of the skin and the production of ECM and α-SMA by fibroblasts ( 50 ). Together with recent observations showing that mast cell deletion ameliorates experimental SSc in vivo ( 47 , 51 ), these results indicate that mast cell targeting in SSc patients may represent an effective therapeutic approach.…”

Section: Emerging Concept: Ssc As An Over-repair Pathologysupporting

confidence: 79%

Innate Immunity in Systemic Sclerosis Fibrosis: Recent Advances

et al. 2018

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Systemic sclerosis (SSc) is a heterogeneous autoimmune disease characterized by three interconnected hallmarks (i) vasculopathy, (ii) aberrant immune activation, and (iii) fibroblast dysfunction leading to extracellular matrix deposition and fibrosis. Blocking or reversing the fibrotic process associated with this devastating disease is still an unmet clinical need. Although various components of innate immunity, including macrophages and type I interferon, have long been implicated in SSc, the precise mechanisms that regulate the global innate immune contribution to SSc pathogenesis remain poorly understood. Recent studies have identified new innate immune players, such as pathogen-recognition receptors, platelet-derived danger-associated molecular patterns, innate lymphoid cells, and plasmacytoid dendritic cells in the pathophysiology of SSc, including vasculopathy and fibrosis. In this review, we describe the evidence demonstrating the importance of innate immune processes during SSc development with particular emphasis on their role in the initiation of pathology. We also discuss potential therapeutic options to modulate innate immune cells or signaling in SSc that are emerging from these recent advances.

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Section: Emerging Concept: Ssc As An Over-repair Pathologysupporting

confidence: 79%

Innate Immunity in Systemic Sclerosis Fibrosis: Recent Advances

et al. 2018

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“…They could demonstrate that a total dose of 1,200 J/cm 2 does obviously not only prevent worsening of dermal fibrosis but also leads to a decrease of fibrotic skin changes (26). A further study by this working group showed in an animal model employing bleomycin- induced scleroderma that UV-A1 (cumulative doses: 1,200 J/cm 2 and 600 J/cm 2 ) is effective as well safe in the management of scleroderma (27). …”

Section: Introductionmentioning

confidence: 99%

Ultraviolet A1 Phototherapy for Fibrosing Conditions

Gambichler

Schmitz

2018

Front. Med.

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In this article we describe efficacy and safety aspects of ultraviolet A1 (UV-A1) phototherapy in fibrosing conditions. UV-A1 is a specific phototherapeutic modality that is defined by a selective spectral range (340–400 nm). UV-A1 includes distinct modes of action qualifying this method for therapy of a variety of conditions, in particular fibrosing skin diseases. Concerning efficacy of UV-A1 phototherapy in fibrosing conditions, the best evidence obtained from randomized controlled trials exists for localized scleroderma. Moreover, fibrosing disorders such as lichen sclerosus and graft-vs.-host disease can be treated successfully by means of UV- A1. Regarding the optimal dosage regimen medium-dose UV-A1 seems to be linked to the best benefit/risk ratio. Possible acute adverse events of UV-A1 phototherapy include erythema and provocation of photodermatoses. Skin ageing and skin cancer formation belong to the chronic adverse events that may occur after long-term UV-A1 phototherapy.

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“…Light at a wavelength of 365 nm has been used in biological studies and the treatment of vitiligo (38,39). Nevertheless, we found obvious toxicity during extended time exposure to this wavelength.…”

Section: Resultsmentioning

confidence: 99%

Generation of a caged lentiviral vector through an unnatural amino acid for photo-switchable transduction

Wang

Tian

et al. 2019

Nucleic Acids Research

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Application of viral vectors in gene delivery is attracting widespread attention but is hampered by the absence of control over transduction, which may lead to non-selective transduction with adverse side effects. To overcome some of these limitations, we proposed an unnatural amino acid aided caging–uncaging strategy for controlling the transduction capability of a viral vector. In this proof-of-principle study, we first expanded the genetic code of the lentiviral vector to incorporate an azido-containing unnatural amino acid (Nϵ-2-azidoethyloxycarbonyl-l-lysine, NAEK) site specifically within a lentiviral envelope protein. Screening of the resultant vectors indicated that NAEK incorporation at Y77 and Y116 was capable of inactivating viral transduction upon click conjugation with a photo-cleavable chemical molecule (T1). Exposure of the chimeric viral vector (Y77-T1) to UVA light subsequently removed the photo-caging group and restored the transduction capability of lentiviral vector both in vitro and in vivo. Our results indicate that the use of the photo-uncage activation procedure can reverse deactivated lentiviral vectors and thus enable regulation of viral transduction in a switchable manner. The methods presented here may be a general approach for generating various switchable vectors that respond to different stimulations and adapt to different viral vectors.

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The safety and efficacy of light emitting diodes-based ultraviolet A1 phototherapy in bleomycin-induced scleroderma in mice

Cited by 7 publications

References 50 publications

Innate Immunity in Systemic Sclerosis Fibrosis: Recent Advances

Innate Immunity in Systemic Sclerosis Fibrosis: Recent Advances

Ultraviolet A1 Phototherapy for Fibrosing Conditions

Generation of a caged lentiviral vector through an unnatural amino acid for photo-switchable transduction

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