Spectral effects of UV on psoriasis

Weatherhead, Sophie; Farr, P.M.; Reynolds, Nick J.

doi:10.1039/c2pp25116g

Cited by 34 publications

(29 citation statements)

References 40 publications

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“…67 The key role of keratinocyte apoptosis in the therapeutic effect of NB-UV-B in psoriasis was recently highlighted by Weatherhead and colleagues. 68,69 Using computational modeling and human studies they demonstrated that keratinocyte apoptosis was sufficient for the clearance of psoriatic plaques.…”

Section: T-cell and Keratinocyte Apoptosismentioning

confidence: 98%

Phototherapy and Photochemotherapy for Psoriasis

Racz,

Prens

2015

Dermatologic Clinics

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Section: T-cell and Keratinocyte Apoptosismentioning

confidence: 98%

Phototherapy and Photochemotherapy for Psoriasis

Racz,

Prens

2015

Dermatologic Clinics

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“…UV-induced keratinocyte apoptosis occurs after irradiation of psoriatic plaque in vivo. The degree of keratinocyte apoptosis may be a useful biomarker indicating clinical response to different UV spectra [117]. A third example is in the effect of keratinocyte apoptosis in the development of arsenic-induced skin cancers.…”

Section: Clinical Implications Of Uv-induced Apoptosismentioning

confidence: 99%

Molecular Mechanisms of UV-Induced Apoptosis and Its Effects on Skin Residential Cells: The Implication in UV-Based Phototherapy

Lee

Wu²,

Hong

et al. 2013

IJMS

194

160

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The human skin is an integral system that acts as a physical and immunological barrier to outside pathogens, toxicants, and harmful irradiations. Environmental ultraviolet rays (UV) from the sun might potentially play a more active role in regulating several important biological responses in the context of global warming. UV rays first encounter the uppermost epidermal keratinocytes causing apoptosis. The molecular mechanisms of UV-induced apoptosis of keratinocytes include direct DNA damage (intrinsic), clustering of death receptors on the cell surface (extrinsic), and generation of ROS. When apoptotic keratinocytes are processed by adjacent immature Langerhans cells (LCs), the inappropriately activated Langerhans cells could result in immunosuppression. Furthermore, UV can deplete LCs in the epidermis and impair their migratory capacity, leading to their accumulation in the dermis. Intriguingly, receptor activator of NF-κB (RANK) activation of LCs by UV can induce the pro-survival and anti-apoptotic signals due to the upregulation of Bcl-xL, leading to the generation of regulatory T cells. Meanwhile, a physiological dosage of UV can also enhance melanocyte survival and melanogenesis. Analogous to its effect in keratinocytes, a therapeutic dosage of UV can induce cell cycle arrest, activate antioxidant and DNA repair enzymes, and induce apoptosis through translocation of the Bcl-2 family proteins in melanocytes to ensure genomic integrity and survival of melanocytes. Furthermore, UV can elicit the synthesis of vitamin D, an important molecule in calcium homeostasis of various types of skin cells contributing to DNA repair and immunomodulation. Taken together, the above-mentioned effects of UV on apoptosis and its related biological effects such as proliferation inhibition, melanin synthesis, and immunomodulations on skin residential cells have provided an integrated biochemical and molecular biological basis for phototherapy that has been widely used in the treatment of many dermatological diseases.

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“…They were located in the basal and suprabasal epidermis. Furthermore, it was demonstrated, that apoptosis occurs also in vivo during routine clinical therapy with NB-UVB and a computational model of psoriatic epidermis revealed that induction of keratinocyte apoptosis (but not inhibition of keratinocyte proliferation) in psoriatic lesions is sufficient for explanation of clearance of psoriatic plaques within the timeframes observed clinically during NB-UVB therapy [34,35]. Based on this study it seems, that, indeed, keratinocytes are the major target of NB-UVB therapeutic efficacy.…”

Section: Narrow Band Uvb (311 Nm) and Apoptosis Of Keratinocytesmentioning

confidence: 99%

Effects of Narrow Band UVB (311 nm) Irradiation on Epidermal Cells

Reich

Mędrek

2013

IJMS

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Ultraviolet radiation (UVR) is known to be one of the most important environmental hazards acting on the skin. It was revealed that chronic exposure to UVR accelerates skin aging, induces immunosuppression and may lead to the development of skin cancers. On the other hand, UVR has been shown to be effective in the treatment of numerous skin diseases and thus, various phototherapy modalities have been developed to date. Narrow-band ultraviolet B (NB-UVB) emitting a light with a peak around 311 nm has been demonstrated to be effective in the treatment of various skin disorders; currently it is one of the most commonly used phototherapy devices. Despite NB-UVB has been developed more than 30 years ago, the exact mechanism of its therapeutic action remains poorly understood. To date, most of NB-UVB effects were attributed to its influence on immune cells; however, nearly 90% of NB-UVB irradiation is absorbed by epidermis and keratinocytes seem to be important players in mediating NB-UVB biological activity. Here, we have reviewed the current data about the influence of NB-UVB on epidermal cells, with a special emphasis on cell proliferation and death.

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Spectral effects of UV on psoriasis

Abstract: Ultraviolet B (UVB) is a highly effective, relatively safe, affordable and widely used therapeutic option for moderate psoriasis.

Cited by 34 publications

References 40 publications

Phototherapy and Photochemotherapy for Psoriasis

Phototherapy and Photochemotherapy for Psoriasis

Molecular Mechanisms of UV-Induced Apoptosis and Its Effects on Skin Residential Cells: The Implication in UV-Based Phototherapy

Effects of Narrow Band UVB (311 nm) Irradiation on Epidermal Cells

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