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Background: We aimed to investigate the prevalence of skin disease among patients with systemic lupus erythematosus (SLE) and determine whether LE skin disease had clinical or serologic correlates with SLE., Methods: We reviewed records of 335 patients with SLE (seen at Mayo Clinic, Rochester, Minnesota, USA) and abstracted skin manifestations, fulfilled mucocutaneous SLE criteria, and clinical and serologic parameters., Results: Of the 231 patients with skin manifestations, 57 (24.7%) had LE-specific conditions, 102 (44.2%) had LE-nonspecific conditions, and 72 (31.2%) had both. LE skin disease was associated with photosensitivity, anti-Smith antibodies, and anti-U1RNP antibodies (all P < 0.001). Patients without LE skin disease more commonly had elevated C-reactive protein levels (P = 0.01). Patients meeting 2-4 mucocutaneous American College of Rheumatology criteria less commonly had cytopenia (P = 0.004) or anti-double-stranded DNA antibodies (P = 0.004). No significant associations were observed for systemic involvement (renal, hematologic, neurologic, and arthritis) when comparing patients with or without LE skin involvement. LE skin involvement was not significantly associated with internal SLE disease flare, number of medications, or overall survival., Conclusions: LE skin disease commonly occurs in patients with SLE. The presence of LE skin disease had no mitigating impact on the severity of SLE sequelae, disease flares, number of medications, or overall survival., (© 2024 Mayo Foundation for Medical Education and Research. International Journal of Dermatology published by Wiley Periodicals LLC on behalf of the International Society of Dermatology.)

Photosensitivity represents an increased inflammatory reaction to sunlight, which can be observed particularly in the autoimmune disease lupus erythematosus. Cutaneous lupus erythematosus (CLE) can be provoked by ultraviolet (UV) radiation and can cause both acute, nonscarring and chronic, scarring skin changes. In systemic lupus erythematosus, on the other hand, provocation by UV radiation can lead to flare or progression of systemic involvement. The etiology of lupus erythematosus is multifactorial and includes genetic, epigenetic and immunologic mechanisms. In this review, we address the effect of UV radiation on healthy skin and photosensitive skin using the example of lupus erythematosus. We describe possible mechanisms of UV-triggered immune responses that could offer therapeutic approaches. Currently, photosensitivity can only be prevented by avoiding UV exposure itself. Therefore, it is important to better understand the underlying mechanisms in order to develop strategies to counteract the deleterious effects of photosensitivity., (© 2024. The Author(s), under exclusive licence to Springer Medizin Verlag GmbH, ein Teil von Springer Nature.)

Solar urticaria is a rare idiopathic photodermatosis. According to the current knowledge its pathogenesis is most likely based on an allergic type I reaction to an autoantigen activated by ultraviolet (UV) radiation or visible light. As many of the patients suffer from severe forms of the disease, it may therefore severely impair the quality of life of those affected. In contrast, polymorphous light eruption is a very common disease, which, according to the current data, can be interpreted as a type IV allergic reaction to a photoallergen induced by UV radiation. As the skin lesions heal despite continued sun exposure, the patients' quality of life is generally not significantly impaired. These two clinically and pathogenetically very different light dermatoses have shared diagnostics by means of light provocation and an important therapeutic option (light hardening). Herein, we present an overview of the clinical picture, pathogenesis, diagnosis and available treatment options for the above-mentioned diseases., (© 2024. The Author(s), under exclusive licence to Springer Medizin Verlag GmbH, ein Teil von Springer Nature.)

Background: Solar urticaria is a rare photodermatosis characterized by rapid-onset sunlight-induced urticaria, but its pathophysiology is not well understood., Objective: We sought to define cutaneous cellular and molecular events in the evolution of solar urticaria following its initiation by solar-simulated UV radiation (SSR) and compare with healthy controls (HC)., Methods: Cutaneous biopsy specimens were taken from unexposed skin and skin exposed to a single low (physiologic) dose of SSR at 30 minutes, 3 hours, and 24 hours after exposure in 6 patients with solar urticaria and 6 HC. Biopsy specimens were assessed by immunohistochemistry and bulk RNA-sequencing analysis., Results: In solar urticaria specimens, there was enrichment of several innate immune pathways, with striking early involvement of neutrophils, which was not observed in HC. Multiple proinflammatory cytokine and chemokine genes were upregulated (including IL20, IL6, and CXCL8) or identified as upstream regulators (including TNF, IL-1β, and IFN-γ). IgE and FcεRI were identified as upstream regulators, and phosphorylated signal transducer and activator of transcription 3 expression in mast cells was increased in solar urticaria at 30 minutes and 3 hours after SSR exposure, suggesting a mechanism of mast cell activation. Clinical resolution of solar urticaria by 24 hours mirrored resolution of inflammatory gene signature profiles. Comparison with available datasets of chronic spontaneous urticaria showed transcriptomic similarities relating to immune activation, but several transcripts were identified solely in solar urticaria, including CXCL8 and CSF2/3., Conclusions: Solar urticaria is characterized by rapid signal transducer and activator of transcription 3 activation in mast cells and involvement of multiple chemotactic and innate inflammatory pathways, with FcεRI engagement indicated as an early event., (Copyright © 2024 The Authors. Published by Elsevier Inc. All rights reserved.)

Photosensitivity is a sensitivity to UV radiation (UVR) commonly found in systemic lupus erythematosus (SLE) patients who have cutaneous disease. Upon even ambient UVR exposure, patients can develop inflammatory skin lesions that can reduce the quality of life. Additionally, UVR-exposed skin lesions can be associated with systemic disease flares marked by rising autoantibody titers and worsening kidney disease. Why SLE patients are photosensitive and how skin sensitivity leads to systemic disease flares are not well understood, and treatment options are limited. In recent years, the importance of immune cell-stromal interactions in tissue function and maintenance is being increasingly recognized. In this review, we discuss SLE as an anatomic circuit and review recent findings in the pathogenesis of photosensitivity with a focus on immune cell-stromal circuitry in tissue health and disease., (Copyright © 2021 by The American Association of Immunologists, Inc.)

Background: Galectin-3 is widely expressed in many immunocytes and epithelial cells including skin keratinocytes. Galectin-3 can regulate immunological or inflammatory processes and plays a proinflammatory role in some disease models. Galectin-3 has a role in disorders related to ultraviolet (UV) photodamage such as apoptosis, skin squamous cell carcinoma and basal cell carcinoma. However, the evidence of galectin-3 in UVB-induced skin inflammation is still limited and the underlying molecular mechanism remains elusive., Objective: We aimed to investigate the effects of galectin-3 in human epidermal keratinocytes and in mice after UVB irradiation., Methods: Primary human epidermal keratinocytes with galectin-3 knockdown were used as the in vitro model. ELISA, QPCR, and western blotting were applied to evaluate the released cytokine, mRNA and protein expression. Histologic analysis, measurement of erythema and transepidermal water loss (TEWL) were applied to evaluate UVB-induced skin damage in galectin-3 knockout mice., Results: In UVB-irradiated human keratinocytes, galectin-3 knockdown downregulated the UVB-induced ASC crosslinking, cleavage of caspase-1, and formation of active IL-1β. Galectin-3 knockdown also decreased UVB-induced production of reactive oxygen species, p38 phosphorylation, and COX2 expression in human keratinocytes. After four days of UVB irradiation, galectin-3 knockout mice showed reduced gross erythema, histologic features of tissue inflammation, quantified levels of erythema and TEWL compared to wild type mice. The skin tissue lysate also showed less expression of active IL-1β and COX2 in galectin-3 knockout mice., Conclusion: Galectin-3 may play a positive regulatory role in UVB-induced skin inflammation., Competing Interests: Declaration of Competing Interest The authors state no conflict of interest., (Copyright © 2020. Published by Elsevier B.V.)

Rosacea is a chronic skin disease characterized by photosensitivity, abnormal dermal vascular behavior, inflammation, and enhanced expression of the antimicrobial peptide LL-37. We observed that dermal endothelial cells in rosacea had an increased expression of VCAM1 and hypothesized that LL-37 could be responsible for this response. The digestion of double-stranded RNA from keratinocytes exposed to UVB blocked the capacity of these cells to induce adhesion molecules on dermal microvascular endothelial cells. However, a synthetic noncoding snoU1RNA was only capable of increasing adhesion molecules on endothelial cells in the presence of LL-37, suggesting that the capacity of UVB exposure to promote both double-stranded RNA and LL-37 was responsible for the endothelial response to keratinocytes. Sequencing of RNA from the endothelial cells uncovered the activation of Gene Ontology (GO) pathways relevant to the human disease, such as type I and II interferon signaling, cell-cell adhesion, leukocyte chemotaxis, and angiogenesis. Functional relevance was demonstrated as double-stranded RNA and LL-37 promoted adhesion and transmigration of monocytes across the endothelial cell monolayers. Gene knockdown of TLR3, RIGI, or IRF1 decreased monocyte adhesion in endothelial cells, confirming the role of the double-stranded RNA recognition pathways. These observations show how the expression of LL-37 can lead to enhanced sensitivity to UVB radiation in rosacea., (Copyright © 2019 The Authors. Published by Elsevier Inc. All rights reserved.)

Cytotoxic T lymphocytes (CTLs) are key players in fighting cancer, and their induction is a major focus in the design of therapeutic vaccines. Yet, therapeutic vaccine efficacy is limited, in part due to the suboptimal vaccine processing by antigen-presenting cells (APCs). Such processing typically takes place via the MHC class II pathway for CD4 T-cell activation and MHC class I pathway for activation of CD8 CTLs. We show that a combination of skin photochemical treatment and immunization, so-called photochemical internalization (PCI) facilitated CTL activation due to the photochemical adjuvant effect induced by photosensitizer, oxygen, and light. Mice were immunized intradermally with antigen and photosensitizer, followed by controlled light exposure. PCI-treated mice showed strong activation of CD8 T cells, with improved IFN-γ production and cytotoxicity, as compared to mice immunized without parallel PCI treatment. Surprisingly, the CD8 T-cell effector functions were not impaired in MHC class II- or CD4 T-cell-deficient mice. Moreover, PCI-based vaccination caused tumor regression independent of MHC class II or CD4 T cells presence in melanoma bearing mice. Together, the data demonstrate that PCI can act as a powerful adjuvant in cancer vaccines, even in hosts with impaired T-helper functions.

UVB-induced skin damage is attributable to reactive oxygen species, which are triggered by intracellular Ca 2+ signals. However, exactly how the reactive oxygen species are triggered by intracellular Ca 2+ upon UVB irradiation remains obscure. Here, we show that UVB induces Ca 2+ signals via sequential generation of the following Ca 2+ messengers: inositol 1,4,5-trisphosphate, nicotinic acid adenine dinucleotide phosphate, and cyclic ADP-ribose. UVB induced H 2 O 2 production through NADPH oxidase 4 activation, which is downstream to inositol 1,4,5-trisphosphate and nicotinic acid adenine dinucleotide phosphate. H 2 O 2 derived from NADPH oxidase 4 activated CD38 to produce cyclic ADP-ribose. UVB first evoked the pannexin channel to release ATP, which acts on P2X7 receptor to generate inositol 1,4,5-trisphosphate. Inhibitors of these messengers, as well as antioxidants, blocked UVB-induced Ca 2+ signals and IL-1β secretion in keratinocytes. Furthermore, ablation of CD38 and NADPH oxidase 4 protected against UVB-induced inflammation and IL-1β secretion in the murine epidermis. These results show that UVB induces IL-1β secretion through cross-talk between Ca 2+ and reactive oxygen species, providing insight towards potential targets against UVB-induced inflammation., (Copyright © 2018 The Authors. Published by Elsevier Inc. All rights reserved.)

Objective: Melatonin and pumpkin seed oil, along with US FDA approved UV filters were incorporated into a formulation for enhancement of UV protection by exerting an antioxidant effect. The objective of this study was to assess the protective effect of this formulation against ultraviolet (UV) radiation-induced photo dermatitis in rats, which is an established model to study the aetiopathogenic mechanisms in psoriasis vulgaris, as the former exhibits the same features to those of clinical psoriasis vulgaris in humans. Materials and methods: The animals were segregated into five groups (6/group) and all received their respective formulations dermally prior to chronic UV irradiation for 28 days. The test, placebo, and standard groups; received the test, placebo, and standard formulations respectively; whereas the positive control group received only UV radiation. A normal control group was also maintained. Disease and treatment status were analyzed using various techniques by euthanizing the rats after 28 days. Results: The test formulation was able to ameliorate the UV-induced increase in skin fold, epidermal thickness, and skin edema; inhibit the reduction of hydroxyproline content and incidence of LPO within the skin tissues of exposed animals. The formulation was also able to inhibit the release of proinflammatory cytokines; IFN-γ, IL-1β, IL-6, and TNF-α; and upregulation of NF-κB and COX-2 genes caused by chronic UV exposure. Conclusion: It can be stated that melatonin included in the newly formulated sunscreen was able to inhibit the induction of photodermatitis via immunoregulation of inflammatory cytokines along with NF-κB and COX-2 genes.

Objective: Skin inflammation and photosensitivity are common in patients with cutaneous lupus erythematosus (CLE) and systemic lupus erythematosus (SLE), yet little is known about the mechanisms that regulate these traits. Here we investigate the role of interferon kappa (IFN-κ) in regulation of type I interferon (IFN) and photosensitive responses and examine its dysregulation in lupus skin., Methods: mRNA expression of type I IFN genes was analysed from microarray data of CLE lesions and healthy control skin. Similar expression in cultured primary keratinocytes, fibroblasts and endothelial cells was analysed via RNA-seq. IFNK knock-out (KO) keratinocytes were generated using CRISPR/Cas9. Keratinocytes stably overexpressing IFN-κ were created via G418 selection of transfected cells. IFN responses were assessed via phosphorylation of STAT1 and STAT2 and qRT-PCR for IFN-regulated genes. Ultraviolet B-mediated apoptosis was analysed via TUNEL staining. In vivo protein expression was assessed via immunofluorescent staining of normal and CLE lesional skin., Results: IFNK is one of two type I IFNs significantly increased (1.5-fold change, false discovery rate (FDR) q<0.001) in lesional CLE skin. Gene ontology (GO) analysis showed that type I IFN responses were enriched (FDR=6.8×10 -04 ) in keratinocytes not in fibroblast and endothelial cells, and this epithelial-derived IFN-κ is responsible for maintaining baseline type I IFN responses in healthy skin. Increased levels of IFN-κ, such as seen in SLE, amplify and accelerate responsiveness of epithelia to IFN-α and increase keratinocyte sensitivity to UV irradiation. Notably, KO of IFN-κ or inhibition of IFN signalling with baricitinib abrogates UVB-induced apoptosis., Conclusion: Collectively, our data identify IFN-κ as a critical IFN in CLE pathology via promotion of enhanced IFN responses and photosensitivity. IFN-κ is a potential novel target for UVB prophylaxis and CLE-directed therapy., Competing Interests: Competing interests: None declared., (© Author(s) (or their employer(s)) 2018. No commercial re-use. See rights and permissions. Published by BMJ.)

Ultraviolet (UV) light is an important environmental trigger for systemic lupus erythematosus (SLE) patients, yet the mechanisms by which UV light impacts disease are not fully known. This review covers evidence in both human and murine systems for the impacts of UV light on DNA damage, apoptosis, autoantigen exposure, cytokine production, inflammatory cell recruitment, and systemic flare induction. In addition, the role of the circadian clock is discussed. Evidence is compared in healthy individuals and SLE patients as well as in wild-type and lupus-prone mice. Further research is needed into the effects of UV light on cutaneous and systemic immune responses to understand how to prevent UV-light mediated lupus flares.

Although immune responses are essential to protect the body from infection, they can also harm tissues. Certain tissues and organs, including the eye, constitute specialized microenvironments that locally inhibit immune reactivity. Dedicator of cytokinesis protein 2 (DOCK2) is a Rac-specific guanine nucleotide exchange factor (GEF) that is predominantly found in hematopoietic cells. DOCK2 plays a key role in immune surveillance because it is essential for the activation and migration of leukocytes. DOCK2 mutations cause severe immunodeficiency in humans. We found that DOCK2-mediated Rac activation and leukocyte migration were effectively inhibited by cholesterol sulfate (CS), but not by cholesterol or other sulfated steroids. CS bound to the catalytic domain of DOCK2 and suppressed its GEF activity. Mass spectrometric quantification revealed that CS was most abundantly produced in the Harderian gland, which provides the lipids that form the oily layer of the tear film. Sulfation of cholesterol is mediated by the sulfotransferases SULT2B1b and, to a lesser extent, SULT2B1a, which are produced from the same gene through alternative splicing. By genetically inactivating Sult2b1 , we showed that the lack of CS in mice augmented ultraviolet- and antigen-induced ocular surface inflammation, which was suppressed by administration of eye drops containing CS. Thus, CS is a naturally occurring DOCK2 inhibitor and contributes to the generation of the immunosuppressive microenvironment in the eye., (Copyright © 2018 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works.)

Background: Photoaggravated allergic contact dermatitis caused by methylchloroisothiazolinone (MCI)/methylisothiazolinone (MI) and MI has been reported., Objectives: To describe the clinical characteristics and results of (photo)patch tests and photo-tests of 10 patients in Belgium and France suffering from photoaggravated contact dermatitis caused by MI., Patients and Methods: Five men and five women, with a median age of 49.5 years, were investigated between January 2012 and February 2017 because of suspected photoaggravated contact dermatitis. Patch tests, photopatch tests and/or photo-tests were performed., Results: Seven patients had positive patch test reactions to both MCI/MI and MI, whereas 3 patients had positive patch test reactions only to MI. In most cases, MI was the (strong) primary sensitizer. Photopatch tests with MCI/MI and/or MI gave stronger reactions than patch tests with these derivatives, indicating photoaggravation. Sensitization probably took place from cosmetics and work-related biocides, whereas elicitation of dermatitis was remarkably often related to airborne exposure to MI present in paints or industrial biocides. Four patients suffered from transient photosensitivity., Conclusion: Photoaggravated allergic contact dermatitis and transient photosensitivity caused by MI is a peculiar clinical presentation of allergic contact dermatitis caused by this preservative, and should be considered in daily clinical practice., (© 2017 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

Introduction: Polymorphic light eruption (PLE) is a common idiopathic photodermatosis that typically presents with pruritic papular or papulovesicular lesions on sun-exposed skin between spring and autumn. In many subjects PLE is mild, and can usually be prevented by the use of broad-spectrum topical sunscreens and a gradual increase in sunlight exposure. However, in some individuals, sunlight exposure results in florid PLE and they often benefit from prophylactic desensitization treatment using phototherapy in early spring, an artificial method that induces a "hardening" phenomenon., Objective: To describe and evaluate the efficacy of a short desensitization protocol, based on a one-month-treatment, administered twice a week with narrow band UVB in subjects with severe polymorphic light eruption (PLE)., Methods: A retrospective, open planned and non-randomized study to assess the efficacy of UVB phototherapy in prevention of polymorphic light eruption., Results: Fifteen subjects diagnosed with severe PLE were treated with the standard protocol in our Photobiology Unit between 2014 and 2015. The effect of hardening was sustained during follow up in 87.5% of desensitization treatments. A statistically significant association (p<0.05) between the years of duration of the PLE and the response to treatment was found., Conclusions: The effect of hardening was maintained in the vast majority of subjects, obtaining a good benefit with no PLE episodes during all the summer. We demonstrate that our standard protocol is effective, and produces a successful outcome for the majority of PLE subjects. Our protocol is shorter than those currently applied, being favourable both for the patient and the physician., (Copyright © 2017 AEDV. Publicado por Elsevier España, S.L.U. All rights reserved.)

Purpose of Review: The photodermatoses represent a group of disorders of sensitivity to light that continue to pose difficulties in diagnosis and management. Photodermatoses are of interest to allergists because many photosensitive skin disorders have immunologic underpinnings, and patients often present to clinic complaining of "allergy" to the sun. We provide a concise reference for allergists on the clinical recognition and management of photodermatitis., Recent Findings: New developments in the understanding of immunomodulatory effects of light have demonstrated normally immunosuppressive responses in the skin to light exposure, and a blunted immunosuppressive response in the pathogenesis of many photodermatoses. Vitamin D plays an important role in immunomodulation and itself may be affected by photodermatoses due to the impact of photoprotective treatment strategies on circulating vitamin D levels. The elucidation of the immunological basis of many photodermatoses may provide guidance for developing new treatment modalities. Further research is necessary to determine the optimal management of vitamin D metabolism in patients with photodermatoses.

Polymorphous light eruption (PLE) is the commonest immuno-mediated photodermatosis. It occurs after solar or artificial UV-light exposure and affects only the sun-exposed areas with preference of the V-area of the chest, of arms and forearms, legs, upper part of the back, and rarely the face. The lesions are itching or burning, and vary morphologically from erythema to papules, vesico-papules and occasionally blisters, plaques, sometimes erythema multiforme-like, insect bite-like wheals and purpura. The clinical manifestations befall within a few hours to days from light exposure, last a few days, and subside in about a week without sequelae. Its diagnosis is based on history, morphology and phototests. PLE is considered as a delayed hypersensitivity response to newly UV induced, but still unidentified, antigen(s). Usually, MED is normal, but the provocative phototests with UVA or UVB reproduce the spontaneous lesions in about 50% of the patients. Broad spectrum sunscreens and antioxidants, photohardening with PUVA or narrow band UVB may be beneficial to prevent the disease. Therapy is based mainly on topical or systemic corticosteroids.

Aim: The purpose of this study was to gain a better understanding of systemic lupus erythematosus (SLE) in Hakka populations., Methods: We studied the demographic, clinical and laboratory characteristics in a cohort of 552 SLE patients diagnosed at the Rheumatology Department in MeiZhou People's Hospital from January 2008 to December 2012. There were 495 women and 57 men (8.7 : 1) with a mean age of 35.3 years (range 12-78 years). The mean age at disease onset and the mean disease duration were 31.8 ± 14.4 years and 3.3 ± 2.8 years, respectively., Results: The most common clinical manifestations were arthritis (61.6%), followed by malar rash (52.7%), photosensitivity (22.8%), mouth ulcers (17.0%) and discoid lupus (14.7%). The prevalence was 46.7% for nephritis (by biopsy), 18.3% for pleuritis, 15.6% for pericarditis and 4.9% for neuropsychiatric manifestations. The most common hematological manifestations were anemia (63.8%), followed by leucopenia (29.0%) and thrombocytopenia (14.9%). Antinuclear antibodies were detected in 99.8% of patients, followed by anti-double-stranded DNA (81.3%), anti-SSA (Sjögren's syndrome antigen A)/Ro (58.7%), anti-ribonucleoprotein (36.8%), anti-Sm (35.7%), and anti-SSB/La (15.0%). Anti-cardiolipin immunoglobulin G (IgG) and IgM were detected in 18.3% and 14.1% of patients, respectively. Active disease and infections were the two major causes of death., Conclusion: The clinical and immunological characteristics of the SLE patients in our study place our population in the middle of the spectrum between other Asian and Caucasian populations., (© 2015 Asia Pacific League of Associations for Rheumatology and Wiley Publishing Asia Pty Ltd.)

Background: We hypothesized that regulatory T cells (Tregs) are involved in the immunological abnormalities seen in patients with polymorphic light eruption (PLE)., Objectives: To investigate the number and suppressive function of peripheral Tregs in patients with PLE compared with healthy controls., Methods: Blood sampling was done in 30 patients with PLE [seeking or not seeking 311-nm ultraviolet (UV)B photohardening] as well as 19 healthy controls at two time points: TP1, March to June (before phototherapy); and TP2, May to August (after phototherapy). We compared the number of CD4(+) CD25(high) CD127(-) FoxP3(+) Tregs by flow cytometry and their function by assessing FoxP3 mRNA levels and effector T cell/Treg suppression assays., Results: Tregs isolated from healthy controls significantly suppressed the proliferation of effector T cells at TP1 by 68% (P = 0·0156). In contrast, Tregs from patients with PLE entirely lacked the capacity to suppress effector T-cell proliferation at that time point. The medical photohardening seen in 23 patients with PLE resulted in a significant increase in the median percentage of circulating Tregs [both as a proportion of all lymphocytes; 65 6% increase (P = 0·0049), and as a proportion of CD4(+) T cells; 32.5% increase (P = 0·0049)]. This was accompanied by an increase in the expression of FoxP3 mRNA (P = 0·0083) and relative immunosuppressive function of Tregs (P = 0·083) comparing the two time points in representative subsets of patients with healthy controls tested. Seven patients with PLE not receiving 311-nm UVB also exhibited an increase in the number of Tregs but this was not statistically significant. No significant differences in Treg numbers were observed in healthy subjects between the two time points., Conclusions: An impaired Treg function is likely to play a role in PLE pathogenesis. A UV-induced increase in the number of Tregs (either naturally or therapeutically) may be a compensatory mechanism by which the immune system counteracts the susceptibility to PLE., (© 2015 The Authors. British Journal of Dermatology published by John Wiley & Sons Ltd on behalf of British Association of Dermatologists.)

Chronic actinic dermatitis/actinic reticuloid (CAD/AR) is an eczematous hypersensitivity reaction to ultraviolet rays that can vary from mild eczematous cases to AR, the most severe cases which may resemble cutaneous T-cell lymphoma. Diagnosis is based on clinical, histopathologic, and photobiologic features. In this study, we characterize the histopathologic and immunohistochemical features of 40 biopsies from 37 patients with established CAD. The cohort included 30 men and 7 women, ranging in age from 38 to 84 years (median, 62 years) and with a median duration of symptoms at presentation of 3 years (range, 1 to 40 years). All patients presented with erythematous lichenified plaques on sun-exposed areas. Severe cases (12/37) had extension to non-exposed areas. Positive photo-testing (20/20) and patch-testing (10/10) results, and cases with a high peripheral blood eosinophila (7/24) and HIV positivity (4/37) were noted. Skin biopsies demonstrated eczematous features including parakeratosis, acanthosis, spongiosis, and prominent dermal fibroplasia. Dermal dendrocytes were prominent in all cases with frequent multinucleated giant cells positive for factor XIIIa and S100 protein. Most cases displayed a brisk lymphocytic infiltrate with subtle exocytosis, atypical lymphocytes, and increased numbers of Langerhans cells, eosinophils, and plasma cells. There was a predominance of CD8 T cells within the epidermis (20/25) and a low CD4:CD8 ratio was noted in 20 of 25 cases. T-cell clonality studies were negative in 10 of 10 cases. CAD/AR may be difficult to distinguish from eczematous variants of cutaneous T-cell lymphoma. Important clues to differentiate both conditions include the identification of prominent dermal dendrocytes with multinucleated giant cells, eosinophils, plasma cells, and a low CD4:CD8 ratio.

The underlying pathomechanisms of lupus erythematosus (LE), a multifactorial autoimmune disease, remain elusive. Due to the clinical evidence demonstrating a clear relationship between ultraviolet (UV) light exposure and skin lesions of LE, photosensitivity has been proven to be an important factor in the pathogenesis of the disease. Standardised photoprovocation with UVA and UVB irradiation has been shown to be a reliable model for evaluating photosensitivity in patients with cutaneous LE (CLE) and analysing the underlying medical conditions of the disease. In this respect, UV irradiation can cause aberrant induction of apoptosis in keratinocytes and contribute to the appearance of excessive apoptotic cells in the skin of CLE patients. Moreover, apoptotic cells that cannot be cleared by phagocytes may undergo secondary necrosis and release proinflammatory compounds and potential autoantigens, which may contribute to the inflammatory micromilieu that leads to formation of skin lesions in the disease. In addition to UV-mediated induction of apoptosis, the molecular and cellular factors that may cause the abnormal long-lasting photoreactivity in CLE include mediators of inflammation, such as cytokines and chemokines. In particular, interferons (IFNs) are important players in the early activation of the immune system and have a specific role in the immunological interface between the innate and the adaptive immune system. The fact that treatment with recombinant type I IFNs (α and β) can induce not only systemic organ manifestations but also LE-like skin lesions provides additional evidence for a pathogenetic role of these IFNs in the disease.

Chronic actinic dermatitis (CAD) is an immunologically mediated photodermatosis characterized by pruritic eczematous and lichenified plaques located predominantly on sun-exposed areas with notable sparing of eyelids, skin folds, and postauricular skin. CAD is thought to be due to secondary photosensitization of an endogenous antigen in the skin. Management of CAD should include strict photoprotection and topical agents, including corticosteroids and calcineurin inhibitors. Other treatments with noted efficacy include oral prednisone, cyclosporine, azathioprine, and mycophenolate mofetil. Photoprotection and avoidance of allergens, if identified, may lead to spontaneous resolution of CAD in 50% of patients over 15 years., (Copyright © 2014 Elsevier Inc. All rights reserved.)

We investigated the characteristics of Chinese SLE patients by analyzing the association between specific autoantibodies and clinical manifestations of 2104 SLE patients from registry data of CSTAR cohort. Significant (P<0.05) associations were found between anti-Sm antibody, anti-rRNP antibody, and malar rash; between anti-RNP antibody, anti-SSA antibody, and pulmonary arterial hypertension (PAH); between anti-SSB antibody and hematologic involvement; and between anti-dsDNA antibody and nephropathy. APL antibody was associated with hematologic involvement, interstitial lung disease, and a lower prevalence of oral ulcerations (P<0.05). Associations were also found between anti-dsDNA antibody and a lower prevalence of photosensitivity, and between anti-SSA antibody and a lower prevalence of nephropathy (P<0.05). Most of these findings were consistent with other studies in the literature but this study is the first report on the association between anti-SSA and a lower prevalence of nephropathy. The correlations of specific autoantibodies and clinical manifestations could provide clues for physicians to predict organ damages in SLE patients. We suggest that a thorough screening of autoantibodies should be carried out when the diagnosis of SLE is established, and repeated echocardiography annually in SLE patients with anti-RNP or anti-SSA antibody should be performed.

Background: Polymorphic light eruption (PLE) is considered to be an autoimmune-mediated skin condition in which the normal ultraviolet (UV)-induced local immunosuppression appears to be absent, leading to recognition of photoinduced autoantigens and subsequent inflammation., Objectives: To investigate T regulatory cells (Tregs) and related immunoregulatory factors in PLE lesions and controls., Methods: Skin biopsies were performed in 13 patients with UVA1-challenged PLE, 12 female patients with chronic discoid lupus erythematosus (CDLE) and 11 healthy controls who had exposure to UVA1. Immunohistochemistry and four-colour immunofluorescence studies were performed., Results: Patients with CDLE and UVA1-exposed controls showed significantly decreased epidermal immunoreactivity for CD1a compared with patients with PLE (P = 0·0001). Four-colour immunofluorescence revealed a median percentage of CD4+CD25+FOXP3+ Tregs of 7·6% (range 3·7-13·6%) in PLE, a median of 11·7% (range 9·5-13·9%) in CDLE and a median of 3·4% (range 0-6·8%) in controls. Compared with UVA1-exposed controls, PLE and CDLE lesions showed significantly decreased transforming growth factor (TGF)-β1 immunoreactivity in the epidermis (P = 0·0003). In PLE lesions, we observed significantly decreased interleukin (IL)-10 expression compared with CDLE (P = 0·022). In the dermis, receptor activator of nuclear factor-κB ligand (RANKL) expression was increased in UVA1-exposed controls compared with PLE and CDLE (P = 0·018)., Conclusions: Similar to CDLE lesions, UVA1-challenged PLE lesions display an altered immunoregulatory network, as indicated by decreased epidermal or dermal expression of TGF-β1, IL-10 and RANKL, and a relatively low number of Tregs, particularly when compared with other inflammatory skin conditions reported in the literature., (© 2013 British Association of Dermatologists.)

Little information exists about the association of anti-SSA/Ro60 and anti-Ro52/TRIM21 with systemic lupus erytematosus (SLE) features. In this work, we analysed the associations of both anti-Ro reactivities with clinical and immunological manifestations in 141 SLE patients. Photosensitivity and xerophtalmia/xerostomia were found to be positively associated with both anti-SSA/Ro60 (P = 0.024 and P = 0.019, resp.) and anti-Ro52/TRIM21 (P = 0.026 and P = 0.022, resp.). In contrast, a negative association was detected regarding anti-phospholipid antibodies, anti-SSA/Ro60 having a stronger effect (P = 0.014) than anti-Ro52/TRIM21. Anti-SSA/Ro60 showed a specific positive association with hypocomplementemia (P = 0.041), mainly with low C4 levels (P = 0.008), whereas anti-Ro52/TRIM21 was found to be positively associated with Raynaud's phenomenon (P = 0.026) and cytopenia (P = 0.048) and negatively associated with anti-dsDNA (P = 0.013). Lymphocytes are involved in the relationship between anti-Ro52/TRIM21 and cytopenia since positive patients showed lower cell levels than negative patients (P = 0.036). In conclusion, anti-SSA/Ro60 and anti-Ro52/TRIM21 showed both common and specific associations in SLE. These data thus increase evidence of the different associations of the two anti-Ro specificities even in a particular disease.

Alveld is a hepatogenous photosensitivity disorder in lambs. The aim of the study was to investigate if alveld affected lambs had a reduced capacity to handle oxidative stress induced from either endogenous and/or exogenous photosensitizers. Serum samples from alveld lambs (n=33) were compared to serum samples from control lambs (n=31) and exposed to a controlled amount of singlet oxygen ((1)O2). The sera from alveld lambs were found to have an impaired ability to deactivate reactive oxygen species (ROS) compared to control sera. A higher degree of initial hemolysis and a higher concentration of the exogenous photosensitizer phytoporphyrin (PP) were detected in alveld sera compared to the controls. The action spectrum for the formation of (1)O2 indicated that PP as well as the endogenous compound protoporphyrin IX (PP IX) may act as in vivo photosensitizers. A relatively high level of iron was detected in pooled serum from alveld lambs that showed a high degree of hemolysis. It was concluded that alveld photosensitivity is likely to be initiated by a photodynamic reaction involving PP and possibly also PP IX followed by a light-independent reaction involving hemoglobin-related products and catalysis by the Fenton reaction., (Copyright © 2013 Elsevier B.V. All rights reserved.)

Photosensitivity disorders in childhood are rare, with the notable exception of overexposure as sunburn, and therefore require a more circumspect approach. Practitioners who treat children are key players in identifying and managing the many photosensitivity disorders that rarely present in childhood. A classic photodistribution of skin findings may suggest photosensitivity, but a correct diagnosis depends on a detailed history correlated with clinical findings., (Copyright © 2013. Published by Elsevier Inc.)

Background: Polymorphous light eruption (PLE) is the most common form of idiopathic photodermatosis. Several morphologic variants of PLE have been described, including a localized form of PLE primarily affecting the helices of the ears. To our knowledge, the presence of lesions on the elbows as the unique manifestation of PLE has not yet been reported. We have studied 9 patients presenting with a recurrent eruption on the elbows, with clinical and histopathologic features indistinguishable from PLE, occurring during springtime. Recently, a peculiar eruption of the elbows, with similar clinical features to our patients, has been proposed as a manifestation of cutaneous lupus erythematosus., Objective: We sought to describe the clinical, histopathological, and immunohistochemical features of this peculiar eruption of the elbows., Methods: Nine patients presenting a recurrent spring eruption on the elbows, collected from April 1989 to June 2012, were retrospectively analyzed. We studied their clinical and histopathological features, and the immunophenotype of the infiltrate., Results: Five patients were men and 4 were women. The mean age was 44.7 years. The lesions consisted of pruriginous, erythematous-edematous papules and plaques, located on both elbows. The eruption appeared during the spring or early summer and recurred seasonally. No associated symptoms were present and the eruption regressed spontaneously or with topical corticosteroids after 7 to 15 days. Histopathologically, the lesions showed typical features of PLE, with variable degree of edema in the papillary dermis, and a papillary and reticular dermal perivascular infiltrate mostly composed of small lymphocytes. Immunohistochemical studies demonstrated strong immunoreactivity for CD2, CD4, and CD8, revealing the infiltrate was composed predominantly of T lymphocytes, with a predominance of T-helper over T-cytotoxic lymphocytes. Immunostaining for CD123 was negative, highlighting the absence of plasmacytoid dendritic cells. Other T- and B-cell markers, including CD30, PD-1, CXCL13, FoxP3, CD79a, and CD56 were also negative., Limitations: Retrospective case series design is a limitation. Phototests were not performed. Results of antinuclear antibodies were only available in 1 patient., Conclusions: We believe this recurrent eruption of the elbows represents a distinctive and localized variant of PLE rather than a peculiar manifestation of cutaneous lupus erythematosus and suggest the term "spring and summer eruption of the elbows" for this peculiar condition. The mechanism of this localization on the elbows, with sparing of other photoexposed areas, remains unknown., (Copyright © 2012 American Academy of Dermatology, Inc. Published by Mosby, Inc. All rights reserved.)

Objective: To determine whether there is any seasonal variation in the activity of systemic lupus erythematosus (SLE) overall and by individual organs., Methods: The study group comprised 2102 patients with SLE who were followed in a prospective longitudinal cohort study. In this cohort, 92.3% of the patients were women. The mean ± SD age of the patients was 47.9 ± 13.9 years, 56.3% were white, 37.1% were African American, and 3.1% were Asian. Global disease activity was recorded by the Safety of Estrogens in Lupus Erythematosus National Assessment - Systemic Lupus Erythematosus Disease Activity Index (SELENA-SLEDAI) and the physician's global assessment. Activity of each organ was also recorded using SLEDAI terms and a visual analog scale (VAS; 0 to 3)., Results: There was significant seasonal variation in photosensitive rash (p < 0.0001), which was more frequent in the spring and summer months (p < 0.0001). There was significantly more arthritis activity in spring and summer, as measured by both SELENA-SLEDAI (p = 0.0057) and the joint VAS (p = 0.0047). A decrease in renal activity was found in the summer months compared to the rest of the year (p = 0.0397). Serositis recorded by VAS had higher activity from August to October (p = 0.0392). Anti-dsDNA levels were significantly higher during October and November (p < 0.0001). There was significant seasonal variation in antiphospholipid antibody levels (p < 0.0001) and lupus anticoagulant (p = 0.0003). We found a significant variation in activity through the year in global disease activity as measured by SELENA-SLEDAI (p = 0.048)., Conclusion: In the Hopkins Lupus Cohort, skin and joint activity is increased during the spring and summer, but other organs have different patterns. These seasonal variations likely reflect environmental factors that influence disease activity, including ultraviolet light and infections.

We present the cases of three siblings with systemic lupus erythematosus (SLE). The diagnosis was made when the sisters were of age 21, 25 and 28 years. They shared some clinical features, including typical facial rash, photosensitivity and Raynaud's phenomenon, and tested positive for antinuclear antibodies. However, their symptoms and clinical courses varied. Human leukocyte antigen (HLA) typing revealed that DR4 and A2 were present in all three sisters, while HLA type A11, B35 and B54 were each found in two of the three sisters. The two elder sisters developed lupus glomerulonephritis 8 and 11 years after the onset of SLE. It is suggested that there are genes responsible for the onset of the disease and also unknown regulatory genes other than HLA result in different phenotypes., (© 2011 Japanese Dermatological Association.)

Lupus erythematosus is a chronic inflammatory autoimmune disease with diverse clinical manifestations ranging from an indolent chronic cutaneous form to a severe potentially life-threatening disease, systemic lupus erythematosus. Discoid lupus erythematosus is a subphenotype of chronic cutaneous lupus erythematosus, characterised by scaly disk-shaped plaques which may be localised or widespread, occurring predominantly on sun-exposed skin and which may rarely progress to squamous cell carcinoma. The pathogenesis of discoid LE comprises complex interactions between multiple susceptibility genes involved in immune responses and clearance of apoptotic cells on the one hand, and environmental factors on the other. Herein, we discuss some aspects of the pathogenesis of discoid lupus erythematosus in relation to ultraviolet radiation and malignant transformation.

A failure to induce immune suppression after UV exposure has been implicated in the pathogenesis of polymorphic light eruption (PLE). This immunological resistance has been linked to an impaired neutrophil infiltration into the skin following UV exposure. Therapeutic photohardening can restore this abnormal neutrophil infiltration in PLE skin and is thought to be responsible for the prophylactic efficacy. The aim of this study was to elucidate the pathogenic mechanism of the described neutrophil deficiency in PLE. Peripheral blood neutrophil responses to the chemoattractants leukotriene B4 (LTB(4)) and formyl-methionyl-leucyl-phenylalanin (fMLP) were investigated in vitro. Samples from 10 patients with PLE before and after 6 weeks of photohardening therapy were assessed. Flow cytometry was used to measure the changes associated with neutrophil activation. We found a significantly reduced neutrophil responsiveness to LTB(4) and fMLP in PLE patients, which was restored to normal levels after phototherapy. Indeed, PLE neutrophil responsiveness to these two chemoattractants after (but not before) phototherapy was similar to that of age- and sex-matched healthy control subjects. This indicates that an abnormal chemotactic potential to neutrophils is a crucial factor in the pathogenesis of PLE. Normalization following photohardening may therefore account for the therapeutic efficacy by restoring UV-induced neutrophil skin infiltration. Our results reveal a completely novel pathogenic mechanism involved in PLE and offer unique targets for therapy., (© 2011 John Wiley & Sons A/S.)

A common feature between patients with a certain group of systemic autoimmune pathologies (SAPs) with rheumatic component, such as lupus erythematosus (LE) in all its forms, is the presence of cutaneous photosensitivity (CP) as well as the existence of autoantibodies (Aabs). These Aabs have also high incidence in other SAPs that do not present CP, like primary Sjögren's syndrome and rheumatoid arthritis. Cutaneous photosensitivity is a condition that consists of an exacerbated skin reaction to solar radiations; its incidence can reach 90% in systemic LE. The mechanisms involved in the development of CP have been extensively studied focusing on different approaches; however, the exact mechanism has not been fully elucidated yet. There are many theories that relate specifically the presence of circulating anti-Ro/SS-A Aabs with the CP phenomenon, though there are several studies which are in disagreement. In this study, we evaluated the Aabs profile (anti-Ro/SS-A 52 kDa, anti-Ro/SS-A 60 kDa, anti-La/SS-B, anti-Sm and ANAs) as well as their titer or reactivity, in a local cohort of 169 patients with SAPs. We related those Aabs profiles and titers with the presence or absence of CP, and we found that there was no significant association between the presence of anti-Ro/SS-A Aabs and the occurrence of CP. On the other hand, a statistically significant positive association was found between CP and high reactivity anti-Sm Aabs, though this fact could be biased by the incidence of both events in SLE patients. To sum up, in the particular population studied, there is no direct relationship between anti-Ro/SS-A Aabs and CP, which is in agreement with some authors and in disagreement with many others, contributing to the endless discussion of this issue.

Objective: We sought to assess if the exclusive use of a broad-spectrum sunscreen can prevent skin lesions in patients with different subtypes of cutaneous lupus erythematosus (CLE) induced by ultraviolet (UV) irradiation under standardized conditions., Methods: A total of 25 patients with a medical history of photosensitive CLE were included in this monocentric, randomized, vehicle-controlled, double-blind, intraindividual study. The test product and its vehicle were applied 15 minutes before UVA and UVB irradiation of uninvolved skin areas on the upper aspect of the back in a random order, and standardized phototesting was performed daily for 3 consecutive days., Results: Characteristic skin lesions were induced by UVA and UVB irradiation in 16 patients with CLE in the untreated area, and 14 patients showed a positive test result in the vehicle-treated area. In contrast, no eruptions compatible with CLE were observed in the sunscreen-treated area in any of the 25 patients. This resulted in significant differences (P < .001) between UV-irradiated sunscreen-treated versus vehicle-treated areas, and between UV-irradiated sunscreen-treated versus untreated areas. Furthermore, a significant difference (P < .05) was observed concerning the age of disease onset and the patient history of photosensitivity. Patients who were younger than 40 years at onset of CLE reported photosensitivity significantly more often than patients with a higher age of disease onset. None of the patients showed any adverse events from application of the test product or the vehicle., Limitations: Data resulting from standardized experimental phototesting might not be transferable to a clinical setting., Conclusion: These results indicate clearly that the use of a highly protective broad-spectrum sunscreen can prevent skin lesions in photosensitive patients with different subtypes of CLE., (Copyright © 2010 American Academy of Dermatology, Inc. Published by Mosby, Inc. All rights reserved.)

Solar urticaria is a rare immunoglobulin E-mediated photodermatosis characterized by the development of a pathognomic wheal and flare within minutes of photoexposure. A 26-year-old man presented with a history of sun-induced urticaria only in areas of pre-existing bruising, which we were able to replicate with monochromator testing. We were also able to demonstrate, by autologous in vitro studies, that a serum factor was responsible.

Hormonal contraceptives are a known but rarely reported cause of photosensitivity. A 35-year-old female developed several episodes of a prurigionous papulovesicular eruption located on sun-exposed areas that resolved without scarring in days. She had been using a transdermal contraceptive (EVRA: norelgestromin and ethinyloestradiol) for 3 years, and once it was stopped, the patient became asymptomatic. She had another episode after the use of oral contraceptives (YAZ: ethinyloestradiol and drospirenone). The biopsy of the lesions showed a spongiotic dermatitis. Minimal erythema dose was diminished when the patient was using EVRA and YAZ and became normal when they were withdrawn. Phototesting with UVA, photopatch testing and blood porphyrins were normal. Antinuclear antibodies were 1/80 initially and were 1/320 6 months later. Anti-deoxyribonucleic acid antibodies, extractable nuclear antigens, anti Ro and Anti La were negative and no systemic symptoms had developed. When all hormonal contraceptives were stopped, the patient became asymptomatic. We report a case of systemic photosensitivity induced by the contraceptive patch. To the best of our knowledge, no other cases induced by transdermal contraceptives have been reported previously.

Cutaneous lupus erythematosus (CLE) is a heterogeneous autoimmune disease involving well-defined skin lesions that can be categorized as acute CLE (ACLE), subacute CLE (SCLE), chronic CLE (CCLE), or intermittent CLE (ICLE). It is commonly accepted that ultraviolet (UV) exposure can induce and exacerbate skin lesions in patients with certain subtypes of CLE. Phototesting with UVA and UVB irradiation using a standardized protocol has proven to be a reliable model to study photosensitivity in CLE and to analyse the underlying pathomechanisms of the disease. In addition to UV-mediated induction of apoptosis, the molecular and cellular factors that may underlie the abnormal long-lasting photoreactivity in CLE include mediators of inflammation such as cytokines and chemokines, inducible nitric oxide (NO) synthase (iNOS), and cellular adhesion molecules. The photosensitivity associated with CLE requires education of the patient about avoidance of excessive sun exposure, continuous photoprotection through physical measures such as protective clothing, and daily application of broad-spectrum sunscreens. Novel approaches to UV-protection, such as alpha-MSH or thymidine dinucleotides, might also have an impact on photosensitivity in patients with CLE. In this review, we summarize the current knowledge about photosensitivity in patients with CLE, including an overview of standardized phototesting procedures, possible molecular pathomechanisms, and photoprotection.

Ultraviolet (UV) light is intricately linked to the functional status of the cutaneous immune system. In susceptible individuals, UV radiation can ignite pathogenic inflammatory pathways leading to allergy or autoimmunity. In others, this same UV radiation can be used as a phototherapy to suppress pathogenic cutaneous immune responses. These vastly different properties are a direct result of UV light's ability to ionize molecules in the skin and thereby chemically alter them. Sometimes these UV-induced chemical reactions are essential, the formation of pre-vitamin D(3) from 7-dehydrocholesterol, for example. In other instances they can be potentially detrimental. UV radiation can ionize a cell's DNA causing adjacent pyrimidine bases to chemically bond to each other. To prevent malignant transformation, a cell may respond to this UV-induced DNA damage by undergoing apoptosis. Although this pathway prevents skin cancer it also has the potential of inducing or exacerbating autoreactive immune responses by exposing the cell's nuclear antigens. Ultraviolet-induced chemical reactions can activate the immune system by a variety of other mechanisms as well. In response to UV irradiation keratinocytes secrete cytokines and chemokines, which activate and recruit leukocytes to the skin. In some individuals UV-induced chemical reactions can synthesize novel antigens resulting in a photoallergy. Alternatively, photosensitizing molecules can damage cells by initiating sunburn-like phototoxic reactions. Herein we review all types of UV-induced skin reactions, especially those involving the immune system., (Published by Elsevier Ltd.)

Background: Previous studies have demonstrated the efficacy and safety of tacrolimus ointment in the treatment of atopic dermatitis (AD); however, few have investigated the effect of tacrolimus on chronic actinic dermatitis (CAD)., Objectives: To investigate the efficacy and safety of tacrolimus ointment on CAD and its mechanism of treatment., Methods: Forty adult patients with CAD were treated with 0.1% tacrolimus ointment. Skin biopsies were performed on 15 patients before and after treatment. The specimens were subjected to immunohistochemical staining with a panel of monoclonal antibodies to CD1a, CD11b, and CC chemokine receptor 7., Results: Among all the 40 patients, two (5%) were clinically cured and 23 (57.5%) achieved excellent results, making a total effective rate of 62.5%; 14 (35%) were improved; and one (2.5%) case was withdrawn due to intolerable itching at the locally applied areas. CD1a, CD11b and CCR7 expression were all significantly down-regulated after topical treatment with tacrolimus., Conclusions: Treatment with topical tacrolimus is effective and safe for chronic actinic dermatitis, probably due to suppression of the function of Langerhans' cells and inflammatory dendritic epidermal cells and their relevant cytokines.

Photosensitivity in childhood is caused by a diverse group of diseases. A specific sensitivity of a child's skin to ultraviolet light is often the first manifestation or a clinical symptom of photodermatosis. It might indicate a serious underlying systemic disease such as lupus erythematosus or dermatomyositis, or a rare group of genetic skin disorders like Xeroderma pigmentosum, Cockayne syndrome, Trichothyodystrophy, Bloom syndrome, Rothmund-Thomson and Kindler syndrome as well as metabolic disorders and cutaneous porphyria. Photosensitivity secondary to topical or systemic agents may also cause photosensitivity in children. Early recognition and prompt diagnosis may prevent complications associated with unprotected exposure to sunlight and avoid actinic injuries that can lead to malignant skin changes.