Sunburn Biology
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Sunburn Biology
Sunburn is an acute biological response of the skin to excessive ultraviolet (UV) radiation, particularly UVB but also wavelengths within the UVA spectrum. Although visible redness is its most familiar feature, sunburn represents a complex tissue response involving DNA photodamage, oxidative stress, inflammatory signaling, vascular changes, programmed cell death, pain sensitization, immune regulation, pigmentation and repair. The severity and character of these responses depend on wavelength, radiation dose, irradiance, skin pigmentation, previous UV exposure and individual biological variation.
UV radiation acts directly on cellular molecules and indirectly through the production of reactive oxygen species. These processes can damage nuclear and mitochondrial DNA, proteins, membrane lipids and other cellular structures. Skin cells respond by activating DNA-repair systems, stress-response pathways, cell-cycle checkpoints and mechanisms that determine whether damaged cells repair themselves, survive, enter senescence or undergo programmed cell death.
UV Radiation and DNA Damage
A major initiating event in sunburn biology is damage to DNA. UVB is particularly effective at producing cyclobutane pyrimidine dimers and 6-4 photoproducts in epidermal DNA. These lesions distort the DNA molecule and interfere with normal transcription and replication. UVA can also contribute to DNA damage, both through oxidative mechanisms and through the formation of some cyclobutane pyrimidine dimers.
Human skin possesses nucleotide-excision-repair mechanisms capable of identifying and removing many UV-induced DNA lesions. The balance between the amount of damage produced and the efficiency of repair strongly influences the biological outcome of exposure. If repair is successful, affected cells may recover. If damage is extensive or persists, checkpoint pathways can halt the cell cycle or trigger apoptosis.
DNA damage is closely related to erythema. Experimental action-spectrum studies have shown similarities between the wavelengths that produce DNA photoproducts and those that produce visible sunburn, supporting the idea that DNA itself is an important initiating chromophore in the erythemal response.
Repeated UV exposure can induce a degree of photoadaptation, including increased pigmentation and epidermal changes. However, visible adaptation does not eliminate DNA damage, and measurable photodamage may occur even after doses too low to produce obvious redness.
Sunburn Cells, p53 and Apoptosis
One of the characteristic cellular features of sunburn is the appearance of apoptotic keratinocytes traditionally called sunburn cells. These cells have accumulated sufficient UV damage to activate controlled cell-death pathways.
The tumor-suppressor protein p53 has a central role in this response. Following UV-induced DNA damage, p53 can promote cell-cycle arrest, DNA repair or apoptosis depending on the severity and persistence of the injury. This helps prevent heavily damaged keratinocytes from surviving and transmitting mutations to daughter cells.
UV-induced apoptosis is not controlled by a single pathway. DNA damage, reactive oxygen species, mitochondrial signaling, death receptors such as Fas, caspases, ceramide signaling, p38 MAP kinase and other stress pathways can contribute. Survival pathways involving EGFR, AKT and related signaling systems may simultaneously oppose apoptosis and allow repair.
Apoptosis therefore represents an important protective mechanism. By eliminating cells with extensive genetic damage, the skin reduces the probability that potentially mutagenic cells will persist. Failure or alteration of these protective mechanisms can contribute to photocarcinogenesis.
Other forms of stress and cell death may also occur. Research has implicated cellular senescence, ferroptosis, autophagy and endoplasmic-reticulum stress in the broader response of epidermal cells to ultraviolet injury.
Erythema and Inflammatory Signaling
The redness associated with sunburn, known as erythema, results from increased cutaneous blood flow and a coordinated inflammatory response. UV-damaged keratinocytes, endothelial cells, immune cells and sensory nerves release numerous mediators that alter blood vessels and recruit inflammatory cells.
Important mediators include prostaglandins, nitric oxide, histamine, tumor necrosis factor alpha, interleukins, chemokines, reactive oxygen species and bioactive lipids. Cyclooxygenase pathways, particularly production of prostaglandin E2, contribute substantially to UVB-induced vasodilation and inflammation.
Neutrophils migrate into UV-damaged skin and participate in the inflammatory response. Keratinocytes also produce cytokines such as IL-1, IL-6, IL-8, IL-10 and TNF-alpha. Inflammasome pathways, including NLRP1 and related signaling systems, can amplify inflammatory cytokine production following cellular injury.
Inflammation develops dynamically over time rather than as a single event. Different cytokines, prostanoids and lipid mediators appear at different stages following exposure, helping initiate, amplify and eventually resolve the sunburn reaction.
Oxidative Stress and Cellular Injury
Ultraviolet radiation can generate reactive oxygen species in epidermal and dermal cells. These reactive molecules damage DNA bases, lipids, proteins, mitochondria and components of the extracellular matrix.
Oxidative stress interacts with inflammatory and apoptotic pathways. Mitochondrial damage can increase production of reactive oxygen species and promote release of pro-apoptotic factors. UV exposure can also deplete antioxidants such as glutathione, reducing the cell's ability to control oxidative injury.
The biological effects of oxidative stress extend beyond acute sunburn. Repeated oxidative injury contributes to collagen degradation, matrix-metalloproteinase activation, cellular senescence and photoaging. Thus, many molecular mechanisms associated with acute sunburn also participate in long-term photodamage.
Pain and Sensory Responses
Sunburn commonly produces tenderness, heat sensitivity and heightened pain. UVB-induced inflammation has therefore become a widely used experimental model for studying inflammatory pain in humans.
Inflammatory mediators sensitize peripheral nociceptors in the irradiated skin. Ion channels including TRPV1 and TRPA1 have been investigated as contributors to this process. Neuropeptides such as substance P and calcitonin gene-related peptide can also participate in neurogenic inflammation and vascular responses.
Pain sensitivity may extend beyond the directly irradiated area. Experimental studies have identified both peripheral and central sensitization following UVB exposure, helping explain why sunburned skin may become unusually sensitive to heat, pressure and mechanical stimulation.
The timing of pain does not necessarily match the timing of visible redness or increased blood flow, indicating that vascular inflammation and sensory sensitization are partly controlled by different biological processes.
Pigmentation and Photoadaptation
Pigmentation modifies the response of human skin to ultraviolet radiation. Melanin absorbs and scatters radiation and can reduce the amount of damaging UV that reaches vulnerable cells in deeper portions of the epidermis.
UV exposure activates communication between keratinocytes and melanocytes. The p53 pathway can stimulate melanogenic signaling following DNA damage, while melanocyte regulators such as MITF and the melanocortin 1 receptor contribute to pigmentation, cell survival and DNA-repair responses.
Several forms of pigmentation occur after UV exposure. UVA can cause rapid immediate pigment darkening, whereas UVB more strongly stimulates delayed melanogenesis. These responses differ in their biological mechanisms and in the amount of photoprotection they provide.
Naturally darker pigmentation is associated with reduced penetration of UV damage into basal epidermal layers and higher erythemal thresholds. Nevertheless, all skin pigmentation types can experience DNA damage from ultraviolet radiation.
Repeated exposure may produce photoadaptation through increased pigmentation, epidermal thickening and changes in DNA-repair capacity. Such adaptation can increase resistance to visible erythema but should not be interpreted as complete protection from molecular damage.
Photoimmunology and Immune Suppression
Ultraviolet radiation affects both innate and adaptive immune responses in the skin. UV-induced immunosuppression involves interactions among DNA damage, keratinocytes, antigen-presenting cells, cytokines, neuroendocrine signals and epidermal photoreceptors.
Langerhans cells are important participants in these responses. UV exposure can alter their behavior and antigen-presenting functions while also influencing regulatory immune pathways.
Urocanic acid, naturally present in the epidermis, has been extensively studied in photoimmunology. Ultraviolet exposure converts trans-urocanic acid into cis-urocanic acid, which can contribute to suppression of cell-mediated immune responses. Serotonin-receptor signaling and other pathways have been proposed as mechanisms for these effects.
Recent research also suggests interactions between the skin microbiome and urocanic-acid metabolism. Certain skin-resident bacteria may metabolize cis-urocanic acid and thereby modify the degree of UV-induced immune suppression.
Immune suppression can have both physiological and pathological consequences. It may help limit excessive inflammatory reactions, but impaired immune surveillance can also contribute to the development of UV-associated skin cancers.
Skin Barrier and Tissue Responses
Sunburn affects the skin as an integrated organ rather than only individual keratinocytes. UV exposure can disrupt tight junctions, alter epidermal lipids and compromise the permeability barrier. Increased transepidermal water loss and other changes in skin biophysical properties may follow irradiation.
Damaged RNA and DNA released from injured cells can function as biological danger signals. For example, UV-damaged RNA can activate Toll-like receptor 3, stimulating inflammatory cytokines while also contributing to subsequent barrier repair.
Keratinocytes can also release extracellular vesicles containing molecular signals from UV-damaged epidermis. These vesicles may communicate with cells in the dermis and activate inflammatory pathways such as STING and inflammasome signaling.
Cutaneous blood vessels and lymphatic vessels are affected as well, contributing to erythema, edema and movement of inflammatory mediators and immune cells through irradiated tissue.
Wavelength, Dose and Individual Variation
The biological effects of ultraviolet radiation depend strongly on wavelength. UVB is generally more efficient at producing erythema and direct DNA photoproducts, while UVA penetrates more deeply and contributes substantially to oxidative stress, pigmentation and cumulative photodamage.
Dose alone does not fully describe UV exposure. Irradiance, or the rate at which radiation is delivered, can influence inflammatory and cellular responses. The same nominal dose may therefore produce somewhat different biological effects under different exposure conditions.
Individual responses also vary with constitutive skin pigmentation, body site, genetics, previous UV exposure, age and cellular repair capacity. Measures such as the minimal erythema dose are commonly used to quantify sensitivity, but visible erythema is an imperfect surrogate for the total amount of molecular damage.
Suberythemal exposure is particularly important because significant DNA and cellular injury can occur without visible sunburn. Absence of redness therefore does not necessarily mean absence of biological damage.
Protection and Biological Repair
The skin possesses multiple defenses against ultraviolet injury. Melanin provides optical protection, antioxidants reduce oxidative stress, DNA-repair enzymes remove photoproducts, cell-cycle checkpoints delay replication and apoptosis eliminates severely damaged cells.
Sunscreens can reduce erythema and also reduce the formation of DNA photoproducts when sufficient protection is provided. Broad-spectrum protection is important because both UVA and UVB contribute to biological damage through different mechanisms.
Experimental research has also explored compounds that influence inflammatory signaling, antioxidants, DNA repair, autophagy and apoptotic pathways. These studies help identify the molecular mechanisms controlling sunburn, although many such experimental interventions are primarily research tools rather than established clinical treatments.
The most effective biological protection remains reduction of excessive ultraviolet exposure before extensive cellular damage occurs.
Long-Term Significance
Sunburn is an acute event, but its molecular consequences can contribute to chronic disease. Surviving cells may retain mutations produced during episodes of ultraviolet injury. Repeated exposure can accumulate genetic and structural damage while promoting photoaging and altering immune surveillance.
UV-associated mutations in tumor-suppressor pathways, combined with chronic inflammatory and proliferative signaling, contribute to the development of skin cancers. Sunburn therefore represents both an immediate inflammatory injury and a visible indicator of underlying molecular events with possible long-term consequences.
The relationship between visible redness and cancer risk is not exact, because DNA damage can occur without sunburn and different wavelengths produce different patterns of injury. Nevertheless, episodes of excessive UV exposure provide clear evidence that the protective capacity of the skin has been exceeded.
Conclusion
Sunburn is a coordinated biological response to ultraviolet injury rather than simply superficial skin redness. UV radiation produces DNA photoproducts, oxidative stress and molecular danger signals that activate repair mechanisms, inflammatory pathways, vascular responses, pigmentation, immune regulation and pain.
Keratinocytes with severe damage may undergo p53-associated apoptosis and become sunburn cells, while inflammatory mediators produce erythema and recruit immune cells. Pigmentation and photoadaptation provide partial protection, but neither completely prevents DNA damage. At the same time, ultraviolet exposure can suppress aspects of cutaneous immunity, disrupt the epidermal barrier and alter communication among epidermal, dermal, immune, vascular, neuronal and microbial components of the skin.
The biology of sunburn therefore illustrates the skin's attempt to balance survival and repair with elimination of irreversibly damaged cells. These protective responses limit injury, but repeated or excessive exposure can overwhelm them, allowing mutations, chronic photodamage, photoaging and carcinogenic changes to accumulate.
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General UV Biology and Acute Skin Responses
Effects of Solar-Simulated (UVB Plus UVA) Radiation on the Skin Microbiome: An Exploratory Study
| Florian Dimmers et al. | Photochemistry and Photobiology | 2026
Reports that erythemal and suberythemal solar-simulated UV exposure can rapidly alter the composition of the human skin microbiome, with some changes persisting for days.
Current Insights and Future Perspectives of Ultraviolet Radiation (UV) Exposure: Friends and Foes to the Skin and Beyond the Skin
| Xiaoyou Tang, Tingyi Yang, Daojiang Yu, Hai Xiong, Shuyu Zhang | Environment International | 2024
Reviews the biological effects of ultraviolet radiation, including DNA damage, oxidative stress, inflammation, immune responses, pigmentation, photoaging, and the pathways linking UV exposure with skin disease.
UV Radiation and the Skin
Provides a broad overview of how UVA and UVB interact with skin, emphasizing DNA photodamage, oxidative stress, melanogenesis, tanning responses, sunburn, photoaging, and photocarcinogenesis.
Acute Effects of UVR on Human Eyes and Skin
| Antony R. Young | Progress in Biophysics and Molecular Biology | 2006
Reviews the acute biological effects of ultraviolet radiation, including erythema, DNA damage, pigmentation, immune modulation, and differences between UVA and UVB responses.
UV-Induced Skin Damage
| Masamitsu Ichihashi et al. | Toxicology | 2003
Reviews molecular and cellular damage caused by solar ultraviolet radiation, including mutations, oxidative stress, inflammation, photoaging, immune effects, and carcinogenesis.
Short-Term and Long-Term Cellular and Molecular Events Following UV Irradiation of Skin: Implications for Molecular Medicine
| Yasuhiro Matsumura, Honnavara N. Ananthaswamy | Expert Reviews in Molecular Medicine | 2002
Connects immediate UV responses such as DNA damage, apoptosis, inflammation, and cell-cycle arrest with longer-term processes including mutation accumulation and skin cancer.
Acute Effects of Ultraviolet Radiation on the Skin
| N. A. Soter | Seminars in Dermatology | 1990
Describes the vascular, inflammatory, cellular, and biochemical changes occurring during the acute skin response to ultraviolet radiation.
DNA Damage, Photoproducts, Genotoxicity and Repair
The Burning Question: Does Exposure to Low Dose and Low Irradiance Ultraviolet Radiation Lead to Cutaneous DNA Damage in People With Skin Types I-III?
| Various authors | Photochemistry and Photobiology | 2026
Examines whether repeated non-burning doses of solar-simulated UV radiation still produce measurable DNA damage in human skin and compares responses at different UV irradiances.
UVB Light Activates an S Phase-Dependent DNA Damage Response in Human Keratinocytes Independent of Oxidative Stress
| Various authors | Toxicological Sciences | 2026
Shows that UVB activates DNA-damage signaling particularly strongly during S phase and distinguishes this response from UVB-induced ROS production.
DNA Containing Cyclobutane Pyrimidine Dimers Is Released From UVB-Irradiated Keratinocytes in a Caspase-Dependent Manner
| Various authors | Journal of Investigative Dermatology | 2022
Shows that fragments of UV-damaged DNA can leave apoptotic keratinocytes, suggesting a mechanism by which cutaneous UV damage may generate extracellular biological signals.
Evaluation of Noninvasive Measurements of Erythema as a Potential Surrogate for DNA Damage in Repetitively UV-Exposed Human Skin
| Various authors | Photochemistry and Photobiology | 2017
Tests how closely visible and instrument-measured redness tracks cyclobutane pyrimidine dimers after repeated UV exposure and photoadaptation.
Determination of the Action Spectrum of UVR-Induced Mitochondrial DNA Damage in Human Skin Cells
| Various authors | Journal of Investigative Dermatology | 2015
Determines which ultraviolet wavelengths are most effective at damaging mitochondrial DNA in keratinocytes and dermal fibroblasts.
Action Spectrum Analysis of UVR Genotoxicity for Skin: Border Wavelengths Between UVA and UVB Can Bring Serious Mutation Loads to Skin
| Various authors | Journal of Investigative Dermatology | 2013
Demonstrates that erythema does not always perfectly predict mutational risk, particularly near the UVA-UVB spectral boundary.
UVA1 Induces Cyclobutane Pyrimidine Dimers but Not 6-4 Photoproducts in Human Skin In Vivo
| Angela Tewari, Robert P. Sarkany, Antony R. Young | Journal of Investigative Dermatology | 2012
Shows that long-wave UVA can produce potentially mutagenic cyclobutane pyrimidine dimers in human skin even though its DNA damage profile differs from UVB.
Nrf1 CNC-bZIP Protein Promotes Cell Survival and Nucleotide Excision Repair Through Maintaining Glutathione Homeostasis
| Various authors | Journal of Biological Chemistry | 2012
Links antioxidant homeostasis with XPC expression, nucleotide-excision repair, and resistance of keratinocytes to UVB-induced apoptosis.
Formation of 8-Hydroxy-2'-Deoxyguanosine in DNA of Cultured Human Keratinocytes by Narrowband and Broadband UVB
| Various authors | British Journal of Dermatology | 2006
Compares oxidative DNA damage produced by clinically relevant narrowband UVB, broadband UVB, and PUVA irradiation.
Apoptosis and Efficient Repair of DNA Damage Protect Human Keratinocytes Against UVB
| M. D'Errico et al. | Cell Death & Differentiation | 2003
Shows how DNA repair and apoptosis operate together to prevent severely UVB-damaged keratinocytes from surviving and propagating mutations.
Ultraviolet-B-Induced Oxidative DNA Base Damage in Primary Normal Human Epidermal Keratinocytes
| Various authors | Journal of Investigative Dermatology | 2003
Shows that UVB increases 8-oxo-dG in normal human keratinocytes through hydrogen peroxide and hydroxyl-radical-dependent oxidative mechanisms.
Measurement of UVB-Induced DNA Damage and Its Consequences in Models of Immunosuppression
| Daniel B. Yarosh et al. | Methods | 2002
Describes approaches for measuring UVB-induced DNA lesions and investigating how DNA damage contributes to the suppression of cutaneous immune responses.
Repeated Ultraviolet Exposure Affords Same Protection Against DNA Photodamage and Erythema in Human Skin Types II and IV but Is Associated With Faster DNA Repair in Skin Type IV
| John M. Sheehan et al. | Journal of Investigative Dermatology | 2002
Compares photoadaptation between lighter and darker skin and finds important differences in DNA-repair kinetics despite comparable acquired protection.
DNA Damage, Death Receptor Activation and Reactive Oxygen Species Contribute to Ultraviolet Radiation-Induced Apoptosis in an Essential and Independent Way
| Dagmar Kulms et al. | Oncogene | 2002
Demonstrates that UV-induced apoptosis is produced by several parallel mechanisms involving nuclear DNA damage, death-receptor signaling, and oxidative stress.
Biological Consequences of Cyclobutane Pyrimidine Dimers
| A. A. Vink, L. Roza | Journal of Photochemistry and Photobiology B: Biology | 2001
Reviews cyclobutane pyrimidine dimers as major UV-induced DNA lesions and discusses their roles in cell death, mutation, immune suppression, and skin carcinogenesis.
Solar-Simulated Skin Adaptation and Its Effect on Subsequent UV-Induced Epidermal DNA Damage
| S. de Winter, A. A. Vink, L. Roza, S. Pavel | Journal of Investigative Dermatology | 2001
Investigates whether repeated low-level solar exposure produces adaptive changes that reduce DNA damage from subsequent ultraviolet irradiation.
The DNA Damage Signal for Mdm2 Regulation, Trp53 Induction, and Sunburn Cell Formation In Vivo Originates From Actively Transcribed Genes
| Various authors | Journal of Investigative Dermatology | 2001
Demonstrates that UV photoproducts in actively transcribed genes provide a major signal triggering p53 activation and formation of apoptotic sunburn cells.
In Situ Repair of Cyclobutane Pyrimidine Dimers and 6-4 Photoproducts in Human Skin Exposed to Solar Simulating Radiation
| V. J. Bykov, J. M. Sheehan, K. Hemminki, A. R. Young | Journal of Investigative Dermatology | 1999
Measures the formation and repair kinetics of major UV photoproducts in human skin following exposure to simulated sunlight.
p53 Induction in Normal Human Skin In Vitro Following Exposure to Solar Simulated UV and UV-B Irradiation
| Various authors | Journal of Photochemistry and Photobiology B | 1999
Demonstrates dose- and time-dependent p53 accumulation after physiologically relevant UVB and simulated sunlight exposure.
The Similarity of Action Spectra for Thymine Dimers in Human Epidermis and Erythema Suggests That DNA Is the Chromophore for Erythema
| Various authors | Journal of Investigative Dermatology | 1998
Provides direct evidence linking the wavelength dependence of epidermal DNA photodamage with the wavelength dependence of human sunburn redness.
The Detection of Cyclobutane Thymine Dimers, (6-4) Photolesions and Dewar Photoisomers in UV-Irradiated Human Skin
Demonstrates the formation and detection of several important classes of UV-induced DNA photoproducts directly in human skin.
The Repair of DNA Damages Induced in Normal Human Skin Fibroblasts Exposed to Simulated Sunlight
| B. S. Rosenstein, D. L. Mitchell | Radiation Research | 1991
Examines how human fibroblasts repair DNA lesions produced by broad-spectrum radiation designed to approximate natural sunlight.
Inhibition of UV Radiation-Induced DNA Damage by a 5-Methoxypsoralen Tan in Human Skin
Investigates whether experimentally induced pigmentation and epidermal adaptation reduce DNA damage during subsequent ultraviolet exposure.
Apoptosis, Cell Death and Sunburn Cells
Long-Wavelength UVA Enhances UVB-Induced Cell Death in Cultured Keratinocytes
| Various authors | Photochemical & Photobiological Sciences | 2021
Shows that UVA1 can delay repair of UVB-induced pyrimidine dimers, promote double-strand breaks, and amplify UVB-induced keratinocyte death.
Keratinocyte Death by Ferroptosis Initiates Skin Inflammation After UVB Exposure
| Various authors | Redox Biology | 2021
Identifies ferroptosis as an important immunogenic form of keratinocyte death following UVB exposure and links it with HMGB1 release and inflammatory recruitment.
Apoptosis, the Only Cell Death Pathway That Can Be Measured in Human Diploid Dermal Fibroblasts Following Lethal UVB Irradiation
| Anne-Sophie Gary, Patrick J. Rochette | Scientific Reports | 2020
Examines cell-death pathways following severe UVB exposure and identifies apoptosis as the measurable death mechanism in irradiated human dermal fibroblasts.
UVB-Induced Anti-Survival and Pro-Apoptotic Effects on HaCaT Human Keratinocytes
| Various authors | International Journal of Molecular Medicine | 2014
Links caspase-9, protein kinase C, Akt, inhibitor-of-apoptosis proteins, and endoplasmic-reticulum stress with UVB-triggered cell death.
UVB-Induced p21 Degradation Promotes Apoptosis of Human Keratinocytes
| Various authors | Photochemical & Photobiological Sciences | 2010
Shows that UVB-mediated degradation of the cell-cycle regulator p21 can increase apoptosis, particularly in p53-defective keratinocytes.
Starting and Propagating Apoptotic Signals in UVB-Irradiated Keratinocytes
| Various authors | Photochemical & Photobiological Sciences | 2009
Reviews the interacting DNA-damage, oxidative, mitochondrial, and receptor-mediated signals determining whether UVB-damaged keratinocytes survive or undergo apoptosis.
ATR-Chk1 Pathway Inhibition Promotes Apoptosis After UV Treatment in Primary Human Keratinocytes
| Various authors | Journal of Investigative Dermatology | 2009
Shows that ATR-Chk1 checkpoint signaling allows some UV-damaged keratinocytes to survive and that inhibiting this pathway increases apoptosis.
Release of Cytokines/Chemokines and Cell Death in UVB-Irradiated Human Keratinocytes
| Various authors | Human Cell | 2008
Measures UVB-induced IL-1beta, IL-6, IL-8, interferon-gamma, G-CSF, MIP-1beta, TNF-alpha, and keratinocyte death.
Apoptosis Induced by Ultraviolet B in HPV-Immortalized Human Keratinocytes Requires Caspase-9 and Is Death Receptor Independent
| Ahmad Daher, Cynthia M. Simbulan-Rosenthal, Dean S. Rosenthal | Experimental Dermatology | 2006
Demonstrates a predominantly mitochondrial, caspase-9-dependent apoptotic pathway following UVB injury in HPV-immortalized keratinocytes.
AKT Delays the Early-Activated Apoptotic Pathway in UVB-Irradiated Keratinocytes via BAD Translocation
| Various authors | Journal of Biological Chemistry | 2006
Shows that IGF-1/Akt signaling can delay UVB-triggered mitochondrial apoptosis by phosphorylating and redistributing the pro-apoptotic protein BAD.
Apoptosis Signal-Regulating Kinase-1 Connects Reactive Oxygen Species to p38 MAPK-Induced Mitochondrial Apoptosis in UVB-Irradiated Human Keratinocytes
| Various authors | Free Radical Biology and Medicine | 2006
Connects early ROS generation with ASK1 and p38 signaling that ultimately drives mitochondrial apoptosis after UVB exposure.
The Sunburn Cell: Regulation of Death and Survival of the Keratinocyte
Reviews competing survival and apoptotic pathways that determine whether an ultraviolet-damaged epidermal keratinocyte becomes a sunburn cell.
Differential Apoptotic Pathways in Human Keratinocyte HaCaT Cells Exposed to UVB and UVC
| Various authors | Apoptosis | 2005
Compares photoproduct formation, caspase activation, and cell-death mechanisms following UVB and UVC irradiation.
Narrow-Band UVB Induces Apoptosis in Human Keratinocytes
| Various authors | Journal of Photochemistry and Photobiology B | 2005
Compares narrowband and broadband UVB and demonstrates dose-dependent apoptotic death in both primary and immortalized human keratinocytes.
Nitric Oxide Inhibits Ultraviolet B-Induced Murine Keratinocyte Apoptosis by Regulating Apoptotic Signaling Cascades
| Various authors | Journal of Dermatological Science | 2005
Shows that nitric oxide can suppress UVB-triggered p53 activity and caspase signaling while maintaining anti-apoptotic Bcl-2 expression.
Epidermal Transit of Replication-Arrested, Undifferentiated Keratinocytes in UV-Exposed XPC Mice: An Alternative to In Situ Apoptosis
| Various authors | Proceedings of the National Academy of Sciences | 2005
Describes an alternative mechanism for eliminating heavily DNA-damaged epidermal cells by physically moving arrested cells out of the basal layer.
Activation of p38 MAPK Is Required for Bax Translocation to Mitochondria, Cytochrome c Release and Apoptosis Induced by UVB
| Various authors | Journal of Biological Chemistry | 2004
Establishes the p38-Bax-mitochondrial pathway as an important mechanism for removing severely UVB-damaged human keratinocytes.
Ultraviolet Irradiation Increases FADD Protein in Apoptotic Human Keratinocytes
| Various authors | Experimental Dermatology | 2003
Identifies increased FADD expression and caspase-8 signaling as components of death-receptor-associated UV-induced keratinocyte apoptosis.
De Novo Ceramide Synthesis Participates in the Ultraviolet B Irradiation-Induced Apoptosis in Undifferentiated Cultured Human Keratinocytes
| Various authors | Journal of Investigative Dermatology | 2003
Shows that UVB stimulates ceramide synthesis and that this lipid signal contributes to apoptosis independently of, but alongside, caspase-3.
Premature Keratinocyte Death and Expression of Marker Proteins of Apoptosis in Human Skin After UVB Exposure
| Various authors | Experimental Dermatology | 2003
Tracks p53, active caspase-3, DNase I, DNA fragmentation, and formation of sunburn cells over time after human skin is exposed to UVB.
Regulation of Apoptosis by p53 in UV-Irradiated Human Epidermis, Psoriatic Plaques and Senescent Keratinocytes
| Jian-Zhong Qin et al. | Oncogene | 2002
Investigates the central role of p53 in controlling apoptosis after ultraviolet damage in normal and altered human keratinocyte populations.
UVB-Mediated Activation of p38 Mitogen-Activated Protein Kinase Enhances Resistance of Normal Human Keratinocytes to Apoptosis by Stabilizing Cytoplasmic p53
| Nadine Chouinard et al. | Biochemical Journal | 2002
Shows that p38 signaling can serve as an adaptive survival response that modifies p53 behavior after ultraviolet injury.
Ultraviolet B Irradiation Induces Apoptosis of Keratinocytes by Direct Activation of Fas Antigen
| Various authors | Journal of Investigative Dermatology | 2002
Provides evidence that UVB can directly aggregate and activate the Fas death receptor independently of Fas ligand, initiating keratinocyte apoptosis.
Hepatocyte Growth Factor/Scatter Factor Inhibits UVB-Induced Apoptosis of Human Keratinocytes via the PI3-Kinase/AKT Pathway
| Michael Mildner et al. | Journal of Biological Chemistry | 2002
Identifies a fibroblast-to-keratinocyte survival signal that protects UV-damaged epidermal cells while maintaining cell-cycle arrest.
The Molecular Determinants of Sunburn Cell Formation
| G. Murphy, A. R. Young, H. C. Wulf, D. Kulms, T. Schwarz | Experimental Dermatology | 2001
Examines the molecular signals responsible for producing apoptotic "sunburn cells" after ultraviolet exposure and their role in eliminating damaged keratinocytes.
Molecular Mechanisms of UV-Induced Apoptosis
| Dagmar Kulms, Thomas Schwarz | Photodermatology, Photoimmunology & Photomedicine | 2000
Reviews pathways by which ultraviolet radiation activates programmed cell death, including DNA damage, death receptors, mitochondrial signaling, and reactive oxygen species.
Molecular Mechanism of Ultraviolet-Induced Keratinocyte Apoptosis
| L. Zhuang, B. Wang, D. N. Sauder | Journal of Interferon & Cytokine Research | 2000
Reviews signaling pathways controlling the apoptotic elimination of keratinocytes damaged by ultraviolet radiation.
Apoptosis and Cytokine Release Induced by Ionizing or Ultraviolet B Radiation in Primary and Immortalized Human Keratinocytes
| Various authors | International Journal of Radiation Biology | 2000
Compares UVB-induced apoptosis and IL-6 release between normal primary keratinocytes and immortalized epithelial cells.
1,25-Dihydroxyvitamin D3, Transforming Growth Factor Beta1, Calcium, and Ultraviolet B Radiation Induce Apoptosis in Cultured Human Keratinocytes
| L. Benassi et al. | Journal of Investigative Dermatology | 1997
Establishes UVB as a strong apoptotic stimulus in normal human keratinocytes and compares it with other physiological regulators of epidermal growth.
Sunburn Cell: Factors Involved in Its Formation
| Kiichiro Danno, Takeshi Horio | Photochemistry and Photobiology | 1987
Investigates biological conditions influencing the production of apoptotic sunburn cells after ultraviolet irradiation.
Inflammation, Erythema, Cytokines and Lipid Mediators
Keratinocyte-Derived Extracellular Vesicles Mediate Crosstalk Between Epidermis and Dermis in UVB-Induced Skin Inflammation
| Yubin Li et al. | Cellular Communication and Signaling | 2024
Shows that UVB-damaged keratinocytes release DNA-rich extracellular vesicles capable of activating STING and inflammasome pathways in dermal macrophages.
Critical Roles of Irradiance in the Regulation of UVB-Induced Inflammasome Activation and Skin Inflammation in Human Skin Keratinocytes
| Te-An Lee et al. | Journal of Photochemistry and Photobiology B: Biology | 2022
Shows that the rate at which a UVB dose is delivered can influence NLRP1 inflammasome activation, ROS production, stress signaling, and inflammatory responses.
UVB-Induced Skin Autoinflammation Due to Nlrp1b Mutation and Its Inhibition by Anti-IL-1beta Antibody
| Various authors | Journal of Investigative Dermatology | 2022
Demonstrates how excessive NLRP1 inflammasome signaling intensifies UVB-induced IL-1beta production and inflammatory skin damage.
Kinetic Profile of Inflammation Markers in Human Skin In Vivo Following Exposure to Ultraviolet B Indicates Synchronic Release of Cytokines and Prostanoids
| Sven R. Quist et al. | Acta Dermato-Venereologica | 2016
Uses human dermal microdialysis to map distinct early, intermediate, and late waves of cytokine and prostanoid production after UVB irradiation.
Ultraviolet Light Exposure Stimulates HMGB1 Release by Keratinocytes
| Various authors | Archives of Dermatological Research | 2013
Identifies HMGB1 as an alarmin released by UV-damaged keratinocytes that may help initiate inflammatory-cell recruitment and cutaneous inflammation.
Ultraviolet Radiation Damages Self Noncoding RNA and Is Detected by TLR3
| Various authors | Nature Medicine | 2012
Demonstrates that UVB-damaged RNA released by keratinocytes activates Toll-like receptor 3 and stimulates TNF-alpha and IL-6 production, helping initiate sunburn inflammation.
Ultraviolet-Radiation Induced Skin Inflammation: Dissecting the Role of Bioactive Lipids
| A. Nicolaou et al. | Chemistry and Physics of Lipids | 2011
Reviews how prostaglandins, platelet-activating factor, endocannabinoids, and other bioactive lipids participate in UV-triggered inflammation and erythema.
UVB and Proinflammatory Cytokines Synergistically Activate TNF-alpha Production in Keratinocytes Through Enhanced Gene Transcription
| Various authors | Journal of Investigative Dermatology | 2009
Shows that UVB and IL-1alpha cooperate to amplify TNF-alpha transcription in keratinocytes, intensifying the cutaneous inflammatory response.
TNF-alpha Production in the Skin
| M. M. Bashir, M. R. Sharma, V. P. Werth | Archives of Dermatological Research | 2009
Reviews TNF-alpha production as an important early component of the inflammatory response of keratinocytes to UVB.
The Sunburn Response in Human Skin Is Characterized by Sequential Eicosanoid Profiles That May Mediate Its Early and Late Phases
| Various authors | FASEB Journal | 2009
Maps prostaglandins and HETEs over 72 hours of human sunburn and links them with erythema, neutrophil infiltration, lymphocyte recruitment, and resolution.
Cytokine Profile in Human Skin in Response to Experimental Inflammation and Administration of a COX Inhibitor
| Various authors | Pain | 2008
Uses UVB-induced human skin inflammation and dermal microdialysis to measure IL-1beta, IL-6, IL-8, IL-10, G-CSF, and other inflammatory mediators.
The Inflammasome Mediates UVB-Induced Activation and Secretion of Interleukin-1β by Keratinocytes
| Lars Feldmeyer et al. | Current Biology | 2007
Identifies inflammasome activation as a mechanism through which UVB-damaged keratinocytes generate the powerful inflammatory cytokine interleukin-1β.
Solar-Simulated Radiation Induces Secretion of IL-6 and Production of Isoprostanes in Human Skin In Vivo
| Michaela Kuhn et al. | Archives of Dermatological Research | 2006
Shows that erythemal solar-simulated radiation increases IL-6 and markers of oxidative lipid damage in living human skin.
In Situ Profiling and Quantification of Cytokines Released During Ultraviolet B-Induced Inflammation
| Various authors | Journal of Immunological Methods | 2006
Combines dermal microdialysis with protein arrays to map the changing cytokine environment during the first day of human UVB inflammation.
Neutrophils Infiltrating Ultraviolet B-Irradiated Normal Human Skin Display High IL-10 Expression
| Gamze Piskin, Jan D. Bos, Marcel B. M. Teunissen | Archives of Dermatological Research | 2005
Shows that UV-recruited neutrophils can produce the immunoregulatory cytokine IL-10, linking acute inflammation with subsequent immune suppression.
Ultraviolet-B-Induced Erythema Is Mediated by Nitric Oxide and Prostaglandin E2 in Combination
| L. E. Rhodes et al. | Journal of Investigative Dermatology | 2001
Provides human evidence that nitric oxide and prostaglandin E2 work together as important mediators of the vasodilation underlying UVB erythema.
Topical Application of a Selective Cyclooxygenase Inhibitor Suppresses UVB-Mediated Cutaneous Inflammation
| Various authors | Journal of Immunology | 2000
Shows that blocking COX-2 reduces UVB-induced edema, neutrophil infiltration, PGE2 production, and sunburn-cell formation.
Effect of Ultraviolet Light on the Release of Neuropeptides and Neuroendocrine Hormones in the Skin
| T. E. Scholzen et al. | Journal of Investigative Dermatology Symposium Proceedings | 1999
Reviews how substance P, CGRP, melanocortins, neurotrophins, and related signaling molecules contribute to UV-induced inflammation and immune regulation.
Photochemistry and Photobiology of Actinic Erythema: Defensive and Reparative Cutaneous Mechanisms
Examines the photochemical events responsible for UV-induced erythema and the antioxidant, pigmentary, and DNA-repair mechanisms that help limit solar injury.
Nitric Oxide and Peroxynitrite Released by UVB-Irradiated Human Endothelial Cells Are Possibly Involved in Skin Erythema and Inflammation
| G. Deliconstantinos, V. Villiotou, J. C. Stavrides | Experimental Physiology | 1996
Identifies reactive nitrogen species generated by UVB-exposed endothelial cells as possible mediators of erythema, vascular changes, and inflammation.
Ultraviolet B Irradiation-Enhanced Interleukin-6 Production and mRNA Expression Are Mediated by IL-1alpha in Cultured Human Keratinocytes
| J. H. Chung et al. | Journal of Investigative Dermatology | 1996
Demonstrates an IL-1alpha-dependent pathway through which UVB stimulates keratinocyte production of the inflammatory cytokine IL-6.
UVB Induces IL-12 Transcription in Human Keratinocytes In Vivo and In Vitro
| Various authors | Photochemistry and Photobiology | 1996
Demonstrates that ultraviolet exposure changes IL-12 expression in human epidermal cells and adds to the complex cytokine response to sunburn.
Induction of IL-10 Gene Expression in Human Keratinocytes by UVB Exposure In Vivo and In Vitro
| C. D. Enk, D. Sredni, A. Blauvelt, S. I. Katz | Journal of Immunology | 1995
Demonstrates that keratinocytes themselves can increase IL-10 expression after UVB exposure and thereby contribute to ultraviolet-induced immunoregulation.
Calcitonin Gene-Related Peptide, Substance P and Nitric Oxide Are Involved in Cutaneous Inflammation Following Ultraviolet Irradiation
| Various authors | European Journal of Pharmacology | 1995
Identifies CGRP, substance P, and nitric oxide as contributors to the prolonged vasodilation and neurogenic inflammation produced by ultraviolet irradiation.
Enhanced Prostaglandin Synthesis After Ultraviolet Injury Is Mediated by Endogenous Histamine Stimulation: A Mechanism for Irradiation Erythema
Shows that histamine signaling can promote increased prostaglandin synthesis following ultraviolet injury and thereby contribute to inflammatory redness.
Human Keratinocytes Are a Source for Tumor Necrosis Factor Alpha: Evidence for Synthesis and Release Upon Stimulation With Ultraviolet Light
| Various authors | Journal of Experimental Medicine | 1990
Provides early evidence that epidermal keratinocytes produce TNF-alpha after UV exposure and that severe human sunburn can increase circulating TNF-alpha.
The Presence of Neutrophils in Human Cutaneous Ultraviolet-B Inflammation
| J. L. Hawk, G. M. Murphy, C. A. Holden | British Journal of Dermatology | 1988
Demonstrates that neutrophils infiltrate human skin after UVB exposure, establishing an important cellular component of the inflammatory sunburn response.
UVA Erythema in Skin: Is It a Sunburn?
| I. Willis, L. Cylus | Journal of Investigative Dermatology | 1977
Investigates the nature of erythema produced by UVA and questions how closely its biological mechanism resembles classic UVB-induced sunburn.
Oxidative Stress, Mitochondria and Cellular Stress
Role of Reactive Oxygen Species in Ultraviolet-Induced Photodamage of the Skin
| Min Wei, Xin He, Na Liu, Hui Deng et al. | Cell Division | 2024
Reviews how UV-generated reactive oxygen species damage DNA, proteins, lipids, mitochondria, and extracellular matrix while activating inflammation and cell-death pathways.
Ultraviolet Light Induced Generation of Reactive Oxygen Species
Explains mechanisms through which ultraviolet wavelengths generate intracellular ROS and how oxidative stress contributes to biological tissue damage.
Mitochondrial Dysfunction and Cellular Stress Progression After Ultraviolet B Irradiation in Human Keratinocytes
| Various authors | Photodermatology, Photoimmunology & Photomedicine | 2008
Tracks ROS generation, mitochondrial membrane depolarization, superoxide formation, nitric oxide production, p53 activity, and apoptosis after UVB exposure.
Molecular Mechanisms for UV-B Irradiation-Induced Glutathione Depletion in Cultured Human Keratinocytes
| Various authors | Photochemistry and Photobiology | 2004
Shows how UVB depletes glutathione and compromises cellular antioxidant defenses through effects on glutathione synthesis machinery.
Detection of Monohydroxyeicosatetraenoic Acids and F2-Isoprostanes in Human UV-Irradiated Skin
| Various authors | Dermatology | 2004
Uses microdialysis and mass spectrometry to measure oxidative lipid products and inflammatory eicosanoids generated in human skin after UVB irradiation.
Pigmentation, Tanning and Photoadaptation
Skin Pigmentation and Its Control: From Ultraviolet Radiation to Stem Cells
| Joseph Michael Yardman-Frank, David E. Fisher | Experimental Dermatology | 2021
Reviews molecular control of pigmentation, including the communication between UV-damaged keratinocytes, melanocytes, stem cells, and signaling pathways that generate tanning.
MITF and UV Responses in Skin: From Pigmentation to Addiction
| Nhu T. Nguyen, David E. Fisher | Pigment Cell & Melanoma Research | 2019
Reviews MITF-centered signaling in melanocytes and its links to UV-induced pigmentation, cellular survival, stress responses, and behavioral effects of UV exposure.
Minimal Erythema Dose, Minimal Persistent Pigment Dose: Which Model for Whitening Products Evaluation Is Better?
| Xiangzi Li et al. | Skin Research and Technology | 2019
Compares erythema and persistent-pigmentation thresholds, providing useful information about wavelength-dependent responses of different skin types.
Cutaneous Pharmacologic cAMP Induction Induces Melanization of the Skin and Improves Recovery From Ultraviolet Injury
| Various authors | Pigment Cell & Melanoma Research | 2019
Shows how cAMP signaling can increase eumelanin, accelerate repair of DNA photolesions, and improve resistance to UV-induced inflammation.
Significance of the Melanocortin 1 Receptor in the DNA Damage Response of Human Melanocytes to Ultraviolet Radiation
| Viki Swope et al. | Pigment Cell & Melanoma Research | 2014
Shows that MC1R signaling enhances DNA-damage recognition and repair responses after ultraviolet exposure.
Effects of Ultraviolet Radiation, Visible Light, and Infrared Radiation on Erythema and Pigmentation: A Review
Compares the wavelength-dependent effects of ultraviolet, visible, and infrared radiation on human skin redness and pigmentation.
The Minimal Melanogenesis Dose/Minimal Erythema Dose Ratio Declines With Increasing Skin Pigmentation Using Solar Simulator and Narrowband Ultraviolet B Exposure
Shows that the relationship between the doses producing pigmentation and erythema changes markedly with baseline skin pigmentation.
Central Role of p53 in the Suntan Response and Pathologic Hyperpigmentation
Demonstrates that UV-induced activation of p53 in keratinocytes stimulates a signaling pathway that increases melanogenesis and contributes to the tanning response.
Photoadaptation During Narrowband Ultraviolet-B Therapy Is Independent of Skin Type: A Study of 352 Patients
| Roy A. Palmer et al. | Journal of Investigative Dermatology | 2006
Uses clinical UVB exposure data to examine how skin becomes increasingly resistant to erythema during repeated irradiation.
Human Skin Responses to UV Radiation: Pigment in the Upper Epidermis Protects Against DNA Damage in the Lower Epidermis and Facilitates Apoptosis
| Various authors | FASEB Journal | 2006
Shows that darker pigmentation reduces DNA damage reaching basal epidermal cells and is associated with more efficient removal of damaged cells through apoptosis.
Minimal Erythema Dose After Multiple UV Exposures Depends on Pre-Exposure Skin Pigmentation
Examines how pre-existing and exposure-induced pigmentation alters the amount of ultraviolet radiation required to produce subsequent erythema.
Physiological Variation in the Erythemal Response to Ultraviolet Radiation and Photoadaptation
| Karen Waterston, Lisa Naysmith, Jonathan L. Rees | Journal of Investigative Dermatology | 2004
Examines differences in erythema susceptibility among body sites and individuals and explores how human skin adapts after repeated UV exposure.
UV-Induced DNA Damage and Melanin Content in Human Skin Differing in Racial/Ethnic Origin
| Various authors | FASEB Journal | 2003
Compares melanin content, minimal erythema dose, DNA photodamage, and lesion removal among human skin pigmentation groups.
Human Pigmentation Genes and Their Response to Solar UV Radiation
| R. A. Sturm | Mutation Research | 1998
Reviews genetic pathways controlling human pigmentation and explains how inherited pigment variation modifies biological responses to solar ultraviolet radiation.
The Relationship Among Minimal Erythema Dose, Minimal Delayed Tanning Dose, and Skin Color
| T. Noda, A. Kawada, M. Hiruma, A. Ishibashi, S. Arai | Journal of Dermatology | 1993
Examines how baseline skin pigmentation relates to the doses required to produce visible erythema and delayed tanning.
An Ultraviolet Radiation Action Spectrum for Immediate Pigment Darkening
| C. Irwin, A. Barnes, D. Veres, K. Kaidbey | Photochemistry and Photobiology | 1993
Defines the wavelengths most effective at causing immediate pigment darkening and helps distinguish UVA-driven pigmentation from UVB-dominated erythema.
The Relation Between Constitutional Skin Color and Photosensitivity Estimated From UV-Induced Erythema and Pigmentation Dose-Response Curves
| W. Westerhof et al. | Journal of Investigative Dermatology | 1990
Quantifies how natural skin color influences susceptibility to ultraviolet-induced redness and pigmentation.
Effect of Cutaneous Hypoxia Upon Erythema and Pigment Responses to UVA, UVB, and PUVA in Human Skin
| M. Auletta, R. W. Gange, O. T. Tan, E. Matzinger | Journal of Investigative Dermatology | 1986
Examines how reduced oxygen availability modifies erythema and pigmentation, helping distinguish oxygen-dependent components of different photobiological responses.
Photobiology of Melanin Pigmentation: Dose/Response of Skin to Sunlight and Its Contents
| M. A. Pathak, D. L. Fanselow | Journal of the American Academy of Dermatology | 1983
Reviews relationships among UV wavelength, dose, melanin production, tanning, photoprotection, and erythema.
Sunburn Protection by Longwave Ultraviolet Radiation-Induced Pigmentation
| K. H. Kaidbey, A. M. Kligman | Archives of Dermatology | 1978
Investigates whether pigmentation induced predominantly by long-wave UVA provides meaningful protection against later erythemal ultraviolet exposure.
Photoimmunology, Immunosuppression and Urocanic Acid
Urocanase-Positive Skin-Resident Bacteria Metabolize cis-Urocanic Acid and Reduce the Immunosuppressive Properties of UVR
| Various authors | Journal of Investigative Dermatology | 2025
Links the skin microbiome with UV-induced immune regulation by showing that particular bacteria metabolize the UV photoproduct cis-urocanic acid.
Langerhans Cells Orchestrate Apoptosis of DNA-Damaged Keratinocytes Upon High-Dose UVB Skin Exposure
| Various authors | European Journal of Immunology | 2024
Shows that Langerhans cells participate in the inflammatory cascade linking high-dose UVB exposure, neutrophil recruitment, DNA damage, and apoptotic removal of keratinocytes.
Photoimmunology: How Ultraviolet Radiation Affects the Immune System
| Jamie J. Bernard, Richard L. Gallo, Jean Krutmann | Nature Reviews Immunology | 2019
Reviews the many ways ultraviolet radiation alters innate and adaptive immunity through DNA damage, mediators, immune cells, microbiota, and systemic signaling.
Langerhans Cells Are Required for UVR-Induced Immunosuppression
| Agatha Schwarz et al. | Journal of Investigative Dermatology | 2010
Demonstrates an important role for epidermal Langerhans cells in initiating the immunosuppressive response to ultraviolet radiation.
Urocanic Acid Suppresses Induction of Immunity in Human Skin
Demonstrates in humans that cis-urocanic acid can reduce the induction of cutaneous cell-mediated immunity.
Ultraviolet Radiation and Immunosuppression
| G. M. Murphy | British Journal of Dermatology | 2009
Reviews the mechanisms by which ultraviolet exposure suppresses cutaneous immune function and considers the implications for infection and skin cancer.
Recent Advances in Urocanic Acid Photochemistry, Photobiology and Photoimmunology
| Neil K. Gibbs, Joanne Tye, Mary Norval | Photochemical & Photobiological Sciences | 2008
Reviews urocanic acid as a major epidermal UV absorber and explores its photochemistry, immune effects, barrier functions, and possible contribution to photocarcinogenesis.
Cis-Urocanic Acid, a Sunlight-Induced Immunosuppressive Factor, Activates Immune Suppression via the 5-HT2A Receptor
| Jeffrey P. Walterscheid et al. | Proceedings of the National Academy of Sciences | 2006
Identifies serotonin 5-HT2A receptor signaling as a mechanism through which UV-generated cis-urocanic acid can suppress immune responses.
Mechanisms of UV-Induced Immunosuppression
| Thomas Schwarz | Keio Journal of Medicine | 2005
Reviews molecular and cellular pathways linking ultraviolet exposure to suppressed contact hypersensitivity and other immune responses.
Ultraviolet B Radiation-Induced Immunosuppression: Molecular Mechanisms and Cellular Alterations
| Nicole Schade, Charlotte Esser, Jean Krutmann | Photochemical & Photobiological Sciences | 2005
Reviews UVB-induced changes in antigen presentation, cytokine signaling, immune-cell activity, and regulatory pathways that suppress cutaneous immunity.
Whole-Body UVB (TL-01) or UVA-1 Irradiation Does Not Alter Immunomodulatory Cytokines in Serum
Tests whether defined ultraviolet treatments produce detectable systemic changes in several circulating immunomodulatory cytokines.
Suppression of Different Phases of Systemic Contact Hypersensitivity by Urocanic Acid Oxidation Products
| A. Kammeyer et al. | Photochemistry and Photobiology | 2004
Shows that UVB-generated oxidation products of epidermal urocanic acid can participate in immune suppression.
Studies to Determine the Immunomodulating Effects of Cis-Urocanic Acid
| Mary Norval, Ali A. El-Ghorr | Methods | 2002
Describes experimental approaches used to investigate the immune-regulating properties of cis-urocanic acid after ultraviolet exposure.
Neuropeptides and Neuroendocrine Hormones in Ultraviolet Radiation-Induced Immunosuppression
| Various authors | Methods | 2002
Reviews CGRP, substance P, nitric oxide, alpha-MSH, and other neuroendocrine signals involved in the immune consequences of ultraviolet exposure.
Isomerization of Urocanic Acid After Ultraviolet Radiation Is Influenced by Skin Pigmentation
| Various authors | Journal of Photochemistry and Photobiology B | 1999
Examines how pigmentation modifies the UV-driven conversion of trans-urocanic acid to immunologically active cis-urocanic acid.
Differential Suppression of the Human Mixed Epidermal Cell Lymphocyte Reaction and Mixed Lymphocyte Reaction by cis-Urocanic Acid
| H. M. Hurks et al. | Photochemistry and Photobiology | 1997
Investigates mechanisms through which cis-urocanic acid alters interactions between epidermal antigen-presenting cells and lymphocytes.
The Role of Urocanic Acid in UV-Induced Immunosuppression: Recent Advances
| M. Norval, N. K. Gibbs, J. Gilmour | Photochemistry and Photobiology | 1995
Reviews evidence linking UV-driven photoisomerization of epidermal urocanic acid with suppression of immune responses.
The Action Spectra for UV-Induced Suppression of MLR and MECLR Show That Immunosuppression Is Mediated by DNA Damage
| H. M. Hurks et al. | Photochemistry and Photobiology | 1995
Uses wavelength-response relationships to support DNA photodamage as a major initiating signal for ultraviolet-induced immune suppression.
Immunosuppression by Ultraviolet B Radiation: Initiation by Urocanic Acid
| F. P. Noonan, E. C. De Fabo | Immunology Today | 1992
Presents evidence for urocanic acid as an early photoreceptor and mediator in the cascade leading from UVB exposure to immune suppression.
Cis-Urocanic Acid as a Mediator of Ultraviolet-Light-Induced Immunosuppression
| S. Gruner et al. | Seminars in Hematology | 1992
Discusses the immunological effects of cis-urocanic acid formed when ultraviolet radiation photoisomerizes trans-urocanic acid in the epidermis.
Urocanic Acid and Immunosuppression
| M. Norval, T. J. Simpson, J. A. Ross | Photochemistry and Photobiology | 1989
Reviews early evidence that the naturally occurring epidermal molecule urocanic acid participates in UV-triggered alterations of immune function.
Suppression of Contact Hypersensitivity by Short-Term Ultraviolet Irradiation: II. The Role of Urocanic Acid
| T. G. Harriott-Smith, W. J. Halliday | Clinical and Experimental Immunology | 1988
Provides experimental evidence that cis-urocanic acid can reproduce important aspects of UV-induced suppression of cell-mediated immunity.
Pain, Hyperalgesia and Sensory Signaling
UVB Irradiation as a Human Pain Model—A Scoping Review
| Almuth Lang et al. | Life | 2026
Reviews the use of controlled UVB irradiation in experimental human pain research, including irradiation protocols, erythema, hyperalgesia, and methodological variation.
Are TRPA1 and TRPV1 Channel-Mediated Signalling Cascades Involved in UVB Radiation-Induced Sunburn?
| Camila Camponogara, Sara Marchesan Oliveira | Environmental Toxicology and Pharmacology | 2022
Reviews evidence implicating sensory TRPA1 and TRPV1 ion channels in the inflammation, oxidative signaling, and pain produced by UVB exposure.
Ultraviolet Radiation on the Skin: A Painful Experience?
| Douglas M. Lopes, Stephen B. McMahon | CNS Neuroscience & Therapeutics | 2016
Reviews the biological mechanisms underlying sunburn pain, including inflammatory mediators, nociceptor sensitization, ion channels, and experimental UVB pain models.
Hyperalgesia and Allodynia to Superficial and Deep-Tissue Mechanical Stimulation Within and Outside of the UVB Irradiated Area in Human Skin
| Silvia Lo Vecchio et al. | Scandinavian Journal of Pain | 2014
Demonstrates that UVB sunburn can alter mechanical pain sensitivity both inside and beyond the directly irradiated region.
The Pattern and Time Course of Somatosensory Changes in the Human UVB Sunburn Model Reveal Peripheral and Central Sensitization
| Burkhard Gustorff et al. | PAIN | 2013
Maps changes in pain sensitivity after UVB exposure and finds evidence for both local peripheral sensitization and broader central nervous-system effects.
Modality-Specific Nociceptor Sensitization Following UV-B Irradiation of Human Skin
| Benjamin Weinkauf, Maurice Main, Martin Schmelz, Roman Rukwied | Journal of Pain | 2013
Examines how UVB inflammation changes nociceptor responsiveness to heat and mechanical stimuli, revealing stimulus-specific mechanisms of sunburn hyperalgesia.
Human Experimental Pain Models 1: The Ultraviolet Light UV-B Pain Model
| James G. Modir, Mark S. Wallace | Methods in Molecular Biology | 2010
Describes controlled UVB irradiation as a reproducible human model for studying inflammatory pain, erythema, and primary hyperalgesia.
Ultraviolet-B Induced Inflammation of Human Skin: Characterisation and Comparison With Traditional Models of Hyperalgesia
| Thomas Bishop et al. | European Journal of Pain | 2009
Characterizes UVB-induced inflammation and pain sensitization in healthy people and compares sunburn with other experimental models of inflammatory pain.
The Effects of Remifentanil and Gabapentin on Hyperalgesia in a New Extended Inflammatory Skin Pain Model in Healthy Volunteers
| Burkhard Gustorff et al. | Anesthesia & Analgesia | 2004
Uses UV-induced inflammatory skin pain to investigate persistent hyperalgesia and test pharmacological modulation of experimentally induced sunburn pain.
The Sunburn Pain Model: The Stability of Primary and Secondary Hyperalgesia Over 10 Hours in a Crossover Setting
| Burkhard Gustorff et al. | Anesthesia & Analgesia | 2004
Evaluates the reproducibility and duration of pain sensitization following experimentally controlled UVB-induced sunburn.
Repeated Subinflammatory Ultraviolet B Irradiation Increases Substance P and Calcitonin Gene-Related Peptide Content
| Franz J. Legat et al. | Neuroscience Letters | 2002
Demonstrates that repeated UVB exposure alters sensory neuropeptide content and enhances subsequent neurogenic inflammation.
Differential Time Courses of Skin Blood Flow and Hyperalgesia in the Human Sunburn Reaction Following Ultraviolet Irradiation of the Skin
| J. Benrath, F. Gillardon, M. Zimmermann | European Journal of Pain | 2001
Shows that vascular inflammation and pain sensitization develop along different time courses after UV exposure, suggesting distinct underlying mediators.
Time Course of UVA- and UVB-Induced Inflammation and Hyperalgesia in Human Skin
| R. T. Hoffmann, M. Schmelz | European Journal of Pain | 1999
Compares UVA and UVB responses and finds that UVB produces delayed hyperemia and pronounced thermal and mechanical hyperalgesia.
Skin Barrier, Vasculature, Photoaging and Structural Damage
Skin Barrier Compromise: A Central Early Event in Ultraviolet Radiation-Induced Skin Pathogenesis
| Tian Wang, Siwen Lu, Lan Sun, Yuxin Cheng | Dermatology | 2026
Examines disruption of the epidermal barrier as an early event linking acute ultraviolet exposure with inflammation and subsequent skin pathology.
Ultraviolet Light Causes Skin Cell Senescence: From Mechanism to Prevention Principle
| Shujia Song, Fuxing Li, Bingxiang Zhao, Min Zhou, Xiaobo Wang | Advanced Biology | 2024
Reviews how ultraviolet-induced DNA damage, oxidative stress, mitochondrial dysfunction, inflammation, and signaling changes drive cellular senescence in skin.
The Impact of Ultraviolet Radiation on Barrier Function in Human Skin: Molecular Mechanisms and Topical Therapeutics
Reviews evidence that ultraviolet radiation can disrupt epidermal barrier integrity through altered lipids, proteins, inflammation, and oxidative damage.
Toll-Like Receptor 3 Activation Is Required for Normal Skin Barrier Repair Following UV Damage
| Various authors | Journal of Investigative Dermatology | 2014
Shows that the same damaged RNA/TLR3 pathway contributing to UV inflammation also helps activate genes required to restore epidermal barrier function.
Ultraviolet Light-Induced Changes of Lymphatic and Blood Vasculature in Skin and Their Molecular Mechanisms
| Mika Sawane, Kentaro Kajiya | Experimental Dermatology | 2012
Reviews how ultraviolet radiation alters cutaneous blood and lymphatic vessels, contributing to erythema, edema, inflammation, and chronic photodamage.
Characterization of Tight Junctions and Their Disruption by UVB in Human Epidermis and Cultured Keratinocytes
| Various authors | Journal of Investigative Dermatology | 2011
Demonstrates that UVB disrupts occludin organization and tight-junction function, providing a mechanism for acute impairment of the epidermal permeability barrier.
Change of Biophysical Properties of the Skin Caused by Ultraviolet Radiation-Induced Photodamage in Koreans
| Various authors | Skin Research and Technology | 2008
Measures erythema, transepidermal water loss, hydration, and recovery after different solar-simulated UV doses.
Acute Skin Alterations Following Ultraviolet Radiation Investigated by Optical Coherence Tomography and Histology
| Thilo Gambichler et al. | Archives of Dermatological Research | 2005
Uses imaging and histology to document structural changes in human skin during the acute response to ultraviolet irradiation.
Ultraviolet Radiation and Skin Aging: Roles of Reactive Oxygen Species, Inflammation and Protease Activation, and Strategies for Prevention of Inflammation-Induced Matrix Degradation
| S. Pillai, C. Oresajo, J. Hayward | International Journal of Cosmetic Science | 2005
Reviews the cascade from UV-generated oxidative stress to inflammatory signaling and matrix-degrading proteases that damage skin structure.
The Spectral Dependence for UVA-Induced Cumulative Damage in Human Skin
| R. Lavker, K. Kaidbey | Journal of Investigative Dermatology | 1997
Investigates how different UVA wavelengths contribute to cumulative structural and cellular injury following repeated exposures.
Cell Signaling, Autophagy and Survival Pathways
Loss of TC-PTP in Keratinocytes Leads to Increased UVB-Induced Autophagy
| Various authors | Experimental Dermatology | 2025
Examines interactions among UVB-induced DNA photoproducts, autophagy, apoptosis, and survival of damaged keratinocytes.
Alternative Autophagy Dampens UVB-Induced NLRP3 Inflammasome Activation in Human Keratinocytes
| Various authors | Journal of Investigative Dermatology | 2024
Identifies a protective autophagy pathway that removes damaged mitochondria and restricts excessive inflammasome activation following UVB exposure.
Dose and Time Effects of Solar-Simulated Ultraviolet Radiation on the In Vivo Human Skin Transcriptome
| M. Bustamante et al. | British Journal of Dermatology | 2020
Maps dose- and time-dependent changes in gene expression following solar-simulated irradiation, revealing the broad molecular response of human skin to UV injury.
Ultraviolet B Radiation Down-Regulates ULK1 and ATG7 Expression and Impairs the Autophagy Response in Human Keratinocytes
| Various authors | Journal of Photochemistry and Photobiology B | 2017
Shows that UVB can suppress autophagic flux and alter important autophagy-related genes in epidermal keratinocytes.
UV Signaling Pathways Within the Skin
| Hongxiang Chen, Qing Y. Weng, David E. Fisher | Journal of Investigative Dermatology | 2014
Explains how ultraviolet radiation activates signaling networks controlling DNA-damage responses, pigmentation, inflammation, survival, apoptosis, and other adaptive reactions.
ER Signaling Is Activated to Protect Human HaCaT Keratinocytes From ER Stress Induced by Environmental Doses of UVB
| Various authors | Biochemical and Biophysical Research Communications | 2010
Shows that relatively low UVB doses activate ATF6, IRE1/XBP1, and protein-quality-control pathways that help keratinocytes cope with ultraviolet stress.
Decreased Ceramide Transport Protein Function Alters Sphingomyelin Production Following UVB Irradiation
| Various authors | Journal of Biological Chemistry | 2008
Links disruption of ceramide transport with ceramide accumulation, decreased sphingomyelin production, and increased keratinocyte apoptosis.
Adaptive Response of Skin to UVB Damage: Role of p53 Protein
| L. Verschooten, L. Declercq, M. Garmyn | International Journal of Cosmetic Science | 2006
Reviews p53-dependent responses to UVB, including cell-cycle arrest, DNA repair, apoptosis, pigmentation, and adaptation to repeated exposure.
Ultraviolet B Radiation Induces Activation of Neutral and Acidic Sphingomyelinases and Ceramide Generation in Cultured Normal Human Keratinocytes
| Cristina Magnoni et al. | Toxicology in Vitro | 2002
Demonstrates rapid ceramide accumulation after UVB and implicates sphingomyelin signaling in growth arrest and apoptosis.
In Situ Demonstration of Phosphorylated c-Jun and p38 MAP Kinase in Epidermal Keratinocytes Following Ultraviolet B Irradiation of Human Skin
| Various authors | Journal of Pathology | 2001
Demonstrates rapid activation of stress-response pathways including JNK/c-Jun and p38 MAP kinase in human epidermis after UVB exposure.
UVB-Induced Epidermal Growth Factor Receptor Phosphorylation Is Critical for Downstream Signaling and Keratinocyte Survival
| Various authors | Photochemistry and Photobiology | 2000
Shows that UVB rapidly activates EGFR-dependent survival signaling and that blocking EGFR increases oxidative stress, apoptosis, and keratinocyte death.
The Expression of Retinoblastoma Protein in Epidermis Is Induced by UVB Exposure
| M. Ueda, N. U. Ahmed, T. Bito, T. Nagano, M. Ichihashi | British Journal of Dermatology | 1996
Demonstrates changes in the retinoblastoma tumor-suppressor pathway after UVB irradiation, providing insight into epidermal cell-cycle responses to DNA injury.
Sunscreens, Photoprotection and Protective Interventions
Handelin Protects Human Skin Keratinocytes Against Ultraviolet B-Induced Photodamage via Autophagy Activation
| Jimin Chu et al. | Archives of Biochemistry and Biophysics | 2023
Uses UVB-stressed keratinocytes to investigate the protective AMPK-mTOR-autophagy pathway and its relationship with cellular damage.
Anti-Inflammatory Effects of Differential Molecular Weight Hyaluronic Acids on UVB-Induced Calprotectin-Mediated Keratinocyte Inflammation
| Various authors | Journal of Dermatological Science | 2022
Examines damage-associated molecular pattern signaling through TLR4 and CD44 during the inflammatory stages following UVB exposure.
Protective Role of Mitochondrial Peroxiredoxin III Against UVB-Induced Apoptosis of Epidermal Keratinocytes
| Various authors | Journal of Biological Chemistry | 2017
Links mitochondrial hydrogen peroxide accumulation with membrane damage, cytochrome-c release, caspase activation, and UVB-induced keratinocyte apoptosis.
Topical Application of Glycolic Acid Suppresses UVB-Induced IL-6, IL-8, MCP-1 and COX-2 Inflammation
| Various authors | Journal of Dermatological Science | 2017
Uses UVB-exposed keratinocytes and mouse skin to investigate NF-kappaB-dependent production of multiple inflammatory mediators.
Photodamage to Human Skin by Suberythemal Exposure to Solar Ultraviolet Radiation Can Be Attenuated by Sunscreens: A Review
| S. Seité, A. Fourtanier, D. Moyal, A. R. Young | British Journal of Dermatology | 2010
Shows that substantial molecular and cellular photodamage can occur below the threshold for visible sunburn and reviews the protective effects of sunscreens.
Hydrolytic Pathway Protects Against Ceramide-Induced Apoptosis in Keratinocytes Exposed to UVB
| Various authors | Journal of Investigative Dermatology | 2010
Shows that ceramidases and sphingosine-1-phosphate metabolism help determine whether UVB-exposed keratinocytes recover or undergo apoptosis.
Ginsenoside Rb1 Suppresses Ultraviolet Radiation-Induced Apoptosis by Inducing DNA Repair
| Various authors | Biological & Pharmaceutical Bulletin | 2009
Shows that enhancement of XPC- and ERCC1-associated nucleotide-excision repair can reduce UV photolesions and keratinocyte apoptosis.
Compound K Suppresses Ultraviolet Radiation-Induced Apoptosis by Inducing DNA Repair in Human Keratinocytes
| Various authors | Archives of Pharmacal Research | 2008
Investigates nucleotide-excision repair proteins XPC and ERCC1 and shows how increasing DNA repair can reduce UV-induced keratinocyte apoptosis.
Green Tea Extract Reduces Induction of p53 and Apoptosis in UVB-Irradiated Human Skin
| Various authors | Experimental Dermatology | 2008
Uses human skin to examine p53 expression, thymidine dimers, TUNEL-positive cells, and sunburn-cell formation following UVB exposure.
Influence of Eicosapentaenoic Acid on Ultraviolet-B Generation of Prostaglandin-E2 and Proinflammatory Cytokines in Human Skin In Vivo
| Hassan Shahbakhti et al. | Photochemistry and Photobiology | 2004
Measures PGE2, IL-1beta, TNF-alpha, IL-6, and IL-8 during experimental human sunburn and examines how omega-3 fatty acids alter these responses.
Autologous Nitric Oxide Protects Mouse and Human Keratinocytes From Ultraviolet B Radiation-Induced Apoptosis
| Various authors | American Journal of Physiology-Cell Physiology | 2003
Demonstrates that endogenous nitric oxide signaling can reduce caspase-3 activation and keratinocyte apoptosis following UVB irradiation.
Broad-Spectrum Sunscreens Offer Protection Against Urocanic Acid Photoisomerization by Artificial Ultraviolet Radiation in Human Skin
| R. G. van der Molen et al. | Journal of Investigative Dermatology | 2000
Uses urocanic-acid photoisomerization as a biological endpoint for evaluating protection from ultraviolet exposure.
Enzyme Plus Light Therapy to Repair DNA Damage in Ultraviolet-B-Irradiated Human Skin
| Various authors | Proceedings of the National Academy of Sciences | 2000
Demonstrates that topical photolyase can remove cyclobutane dimers from UVB-exposed human skin and reduce erythema, sunburn cells, and immune suppression.
Protection by UVA and UVB Sunscreens Against In Situ Dipyrimidine Photolesions in Human Epidermis Is Comparable to Protection Against Sunburn
| Various authors | Journal of Investigative Dermatology | 2000
Demonstrates a close relationship between sunscreen protection from erythema and protection from UV-induced thymine dimers and 6-4 photoproducts.
The Time of Onset and Duration of 5-Methoxypsoralen Photochemoprotection From UVR-Induced DNA Damage in Human Skin
| C. A. Chadwick, C. S. Potten, A. J. Cohen, A. R. Young | British Journal of Dermatology | 1994
Measures how acquired pigmentation and epidermal thickening influence protection against subsequent UV-induced DNA damage and how long that protection persists.
Dietary Fish-Oil Supplementation in Humans Reduces UVB-Erythemal Sensitivity but Increases Epidermal Lipid Peroxidation
| Various authors | Journal of Investigative Dermatology | 1994
Demonstrates that changing epidermal fatty-acid composition alters the human sunburn threshold while simultaneously affecting oxidative lipid damage.
Action Spectra, Exposure Metrics, Models and Measurement
Characterization of a Human Skin Equivalent Model to Study the Effects of Ultraviolet B Radiation on Keratinocytes
| Various authors | Tissue Engineering | 2014
Describes a reconstructed human epidermal model showing UVB-induced p53 activation, cytokine production, and apoptotic sunburn cells.
Human Erythema and Matrix Metalloproteinase-1 mRNA Induction In Vivo Share an Action Spectrum
| Various authors | Photochemical & Photobiological Sciences | 2012
Finds similar wavelength dependence for erythema and MMP-1 induction, suggesting shared initiating chromophores including DNA.
An Action Spectrum for TNF-alpha Protein in Human Skin In Vivo Suggests That Basal-Layer Epidermal DNA Is the Chromophore
| Susan L. Walker, Antony R. Young | Proceedings of the National Academy of Sciences | 2007
Shows that the wavelength dependence of TNF-alpha production closely matches DNA photodamage in basal epidermal cells.
The Effect of UVA1, UVB and Solar-Simulated Radiation on p53 Activation and p21
| Various authors | British Journal of Dermatology | 2005
Compares p53 phosphorylation and p21 responses after biologically equivalent UVA1, narrowband UVB, and solar-simulated exposures.
Action Spectrum for Erythema in Humans Investigated With Dye Lasers
| A. Anders, H. J. Altheide, M. Knalmann et al. | Photochemistry and Photobiology | 1995
Uses narrow spectral bands to determine the relative effectiveness of different ultraviolet wavelengths at producing erythema in human skin.
Action Spectra for Human Skin Cells: Estimates of Relative Cytotoxicity of Middle UV, Near UV, Violet and Sunlight on Epidermal Keratinocytes
| R. M. Tyrrell, M. Pidoux | Cancer Research | 1987
Compares the cytotoxic effectiveness of different ultraviolet and visible wavelengths in human epidermal keratinocytes.
UV Light Sensitivity of the Skin—Possibilities and Limits of Clinical Diagnosis
| N. Haake, N. Buhles, P. Altmeyer | Zeitschrift für Hautkrankheiten | 1987
Discusses assessment of individual ultraviolet sensitivity and the strengths and limitations of clinical phototesting methods.
Skin Cancer and Photocarcinogenesis
Ultraviolet Radiation-Induced Immunosuppression and Its Relevance for Skin Carcinogenesis
| Prue H. Hart, Mary Norval | Photochemical & Photobiological Sciences | 2018
Explains how UV-induced immune suppression can impair antitumor surveillance and thereby contribute to the development of skin cancer.
Ultraviolet A Radiation: Its Role in Immunosuppression and Carcinogenesis
Reviews evidence that UVA contributes substantially to sunlight-induced immune suppression through oxidative mechanisms and may thereby promote skin carcinogenesis.
COX-2 Expression Is Induced by UVB Exposure in Human Skin: Implications for the Development of Skin Cancer
| Various authors | Carcinogenesis | 1998
Shows that acute UVB irradiation strongly increases cyclooxygenase-2 and prostaglandin production in human keratinocytes and human skin.
Sunlight and Carcinogenesis: Expression of p53 and Pyrimidine Dimers in Human Skin Following UVA I, UVA I + II and Solar Simulating Radiations
| Various authors | International Journal of Cancer | 1998
Compares the epidermal DNA-damage and p53 responses produced by different ultraviolet spectral regions at biologically equivalent doses.
Ultraviolet Irradiation, Systemic Immunosuppression and Skin Cancer: Role of Urocanic Acid
| J. J. Finlay-Jones, P. H. Hart | Australasian Journal of Dermatology | 1997
Discusses urocanic acid as a UV-responsive epidermal molecule capable of contributing to systemic immunosuppression and possibly photocarcinogenesis.
Sunlight and Sunburn in Human Skin Cancer: p53, Apoptosis, and Tumor Promotion
| D. E. Brash et al. | Journal of Investigative Dermatology Symposium Proceedings | 1996
Links sunburn biology with p53 mutation, apoptosis, clonal expansion of damaged cells, and the development of sunlight-associated skin cancers.
Excision Repair of Pyrimidine Dimers Induced by Simulated Solar Radiation in Skin of Patients With Basal Cell Carcinoma
Investigates nucleotide-excision repair of solar-radiation-induced pyrimidine dimers in human skin in relation to basal cell carcinoma susceptibility.
