Nitric Oxide-Mediated Depletion of Langerhans Cells from the Epidermis May Be Involved in UVA Radiation-Induced Immunosuppression

Yuen, Kylie S.; Nearn, Malcolm R.; Halliday, Gary M.

doi:10.1006/niox.2001.0414

Cited by 38 publications

(33 citation statements)

References 37 publications

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“…Although the involvement of LC in suppression of recall immunity is less clear, we find that immunosuppressive doses of ssUV reduce the number of these cells in human skin (Kuchel et al, 2003(Kuchel et al, , 2005. UVA also reduces the number (Yuen et al, 2002) and function (Clement-Lacroix et al, 1996) of epidermal LC. It is possible that UVB and UVA both cause similar molecular and cellular changes such as UCA isomerization or LC damage but over different time courses with an eventual cumulative effect making ssUV more immunosuppressive than either waveband alone.…”

Section: Discussionmentioning

confidence: 83%

“…But UVA mediates much of its damage by production of reactive oxygen species (ROS) (Halliday, 2005), producing a different genetic lesion, 8-hydroxy-2 0 -deoxyguanine (Cadet et al, 2005). It is not known whether 8-hydroxy-2 0 -deoxyguanine initiates UVA-induced immunosuppression; however, ROS are involved in mice (Yuen et al, 2002) and humans (Clement-Lacroix et al, 1996;Kuchel et al, 2003). It is possible that discrete downstream events resulting from different initiating events such as distinct types of genetic damage may be responsible for the different times taken for UVB and UVA to suppress immunity to antigen, and that these may eventually interact to make ssUV more immunosuppressive than either waveband alone.…”

Section: Discussionmentioning

confidence: 98%

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Sunlight-Induced Immunosuppression in Humans Is Initially Because of UVB, Then UVA, Followed by Interactive Effects

Poon

Barnetson

Halliday

2005

Journal of Investigative Dermatology

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Solar-simulated ultraviolet radiation (ssUV) suppresses immunity in humans. The ultraviolet B (UVB) waveband is recognized as immunosuppressive; however the relative significance of UVA to ssUV immunosuppression is unknown. We created dose and time-response curves for UVB-, UVA-, and ssUV-induced suppression of memory immunity to nickel in humans. UVB caused immunosuppression within 24 h. UVA immunosuppression required 48 h and was normalized by 72 h. UVB alone accounts for ssUV immunosuppression at 24 h, but both UVB and UVA contributed at 48 h. By 72 h neither waveband accounted for ssUV immunosuppression. An interaction between these wavebands was therefore the major contributor. To confirm this dose-response curves were used to determine immune protection factors (IPF) for sunscreens with nickel challenge 72 h following ssUV. A sunscreen with good UVA protection had an IPF twice that of a poor UVA protector, despite providing similar protection from sunburn. Thus UVA was a major contributor to ssUV-induced immunosuppression at 72 h but only with the cooperation of UVB. Hence, UVB initiates immunosuppressive signals within 24 h, followed by UVA at 48 h, then an interaction between UVB and UVA. By 72 h following ssUV exposure, neither UVB nor UVA, but an interaction between them is the major cause of sunlight-induced immunosuppression.

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Section: Discussionmentioning

confidence: 83%

Section: Discussionmentioning

confidence: 98%

Sunlight-Induced Immunosuppression in Humans Is Initially Because of UVB, Then UVA, Followed by Interactive Effects

Poon

Barnetson

Halliday

2005

Journal of Investigative Dermatology

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“…Due to the far greater proportion of UVA1 in solar UV, the relative solar immune suppressive efficiency of UVA1 was threefold higher than that of UVB at doses received during normal daily activities [15]. UVA1 induced alteration of adaptive immunity can involve cellular and molecular mechanisms such as isomerization of urocanic acid [71], morphological alteration and depletion of Langerhans cells via the generation of ROS and reactive nitrogen species [72]–[74] and reduction of calcineurin activity due to ROS [75].…”

Section: Discussionmentioning

confidence: 99%

Diversity of Biological Effects Induced by Longwave UVA Rays (UVA1) in Reconstructed Skin

et al. 2014

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Despite their preponderance amongst the ultraviolet (UV) range received on Earth, the biological impacts of longwave UVA1 rays (340–400 nm) upon human skin have not been investigated so thoroughly. Nevertheless, recent studies have proven their harmful effects and involvement in carcinogenesis and immunosuppression. In this work, an in vitro reconstructed human skin model was used for exploring the effects of UVA1 at molecular, cellular and tissue levels. A biological impact of UVA1 throughout the whole reconstructed skin structure could be evidenced, from morphology to gene expression analysis. UVA1 induced immediate injuries such as generation of reactive oxygen species and thymine dimers DNA damage, accumulating preferentially in dermal fibroblasts and basal keratinocytes, followed by significant cellular alterations, such as fibroblast apoptosis and lipid peroxidation. The full genome transcriptomic study showed a clear UVA1 molecular signature with the modulation of expression of 461 and 480 genes in epidermal keratinocytes and dermal fibroblasts, respectively (fold change> = 1.5 and adjusted p value<0.001). Functional enrichment analysis using GO, KEGG pathways and bibliographic analysis revealed a real stress with up-regulation of genes encoding heat shock proteins or involved in oxidative stress response. UVA1 also affected a wide panel of pathways and functions including cancer, proliferation, apoptosis and development, extracellular matrix and metabolism of lipids and glucose. Strikingly, one quarter of modulated genes was related to innate immunity: genes involved in inflammation were strongly up-regulated while genes involved in antiviral defense were severely down-regulated. These transcriptomic data were confirmed in dose-response and time course experiments using quantitative PCR and protein quantification. Links between the evidenced UVA1-induced impacts and clinical consequences of UVA1 exposure such as photo-aging, photo-immunosuppression and cancer are discussed. These early molecular events support the contribution of UVA1 to long term harmful consequences of UV exposure and underline the need of an adequate UVA1 photoprotection.

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“…Tempol was effective in protecting cells (Weaver & Chon, 1966), skin (Bernstein et al, 2001; Yuen et al, 2002) and dermal fibroblasts (Yan et al, 2005) from UV light damage or photoaging. A tempol derivative was more effective than common ingredients of sunscreen formulations in protecting against UV damage (Damiani et al, 2002).…”

Section: Additional Actions Of Tempolmentioning

confidence: 99%

Effects of tempol and redox-cycling nitroxides in models of oxidative stress

Wilcox

2010

Pharmacology & Therapeutics

411

360

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Tempol is a redox cycling nitroxide that promotes the metabolism of many reactive oxygen species (ROS) and improves nitric oxide bioavailability. It has been studied extensively in animal models of oxidative stress. Tempol has been shown to preserve mitochondria against oxidative damage and improve tissue oxygenation. Tempol improved insulin responsiveness in models of diabetes mellitus and improved the dyslipidemia, reduced the weight gain and prevented diastolic dysfunction and heart failure in fat-fed models of the metabolic syndrome. Tempol protected many organs, including the heart and brain, from ischemia/reperfusion damage. Tempol prevented podocyte damage, glomerulosclerosis, proteinuria and progressive loss of renal function in models of salt and mineralocorticosteroid excess. It reduced brain or spinal cord damage after ischemia or trauma and exerted a spinal analgesic action. Tempol improved survival in several models of shock. It protected normal cells from radiation while maintaining radiation sensitivity of tumor cells. Its paradoxical pro-oxidant action in tumor cells accounted for a reduction in spontaneous tumor formation. Tempol was effective in some models of neurodegeneration. Thus, tempol has been effective in preventing several of the adverse consequences of oxidative stress and inflammation that underlie radiation damage and many of the diseases associated with aging. Indeed, tempol given from birth prolonged the life span of normal mice. However, presently tempol has been used only in human subjects as a topical agent to prevent radiation-induced alopecia.

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Nitric Oxide-Mediated Depletion of Langerhans Cells from the Epidermis May Be Involved in UVA Radiation-Induced Immunosuppression

Cited by 38 publications

References 37 publications

Sunlight-Induced Immunosuppression in Humans Is Initially Because of UVB, Then UVA, Followed by Interactive Effects

Sunlight-Induced Immunosuppression in Humans Is Initially Because of UVB, Then UVA, Followed by Interactive Effects

Diversity of Biological Effects Induced by Longwave UVA Rays (UVA1) in Reconstructed Skin

Effects of tempol and redox-cycling nitroxides in models of oxidative stress

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