Suppression of UV‐induced damage by a liposomal sunscreen: a prospective,open‐label study in patients with cutaneous lupus erythematosus and healthy controls

This study aimed to determine whether a broad‐spectrum liposomal sunscreen with a very high sun protection factor (Daylong actinica) can prevent damage induced by ultraviolet (UV) irradiation in patients with cutaneous lupus erythematosus (CLE) and healthy controls (HCs) under standardised conditions. In 20 patients with CLE and 10 HCs, defined areas of sunscreen‐untreated and sunscreen‐treated skin on the upper back were irradiated with combined UVA/UVB light. Disease‐specific skin lesions were induced by UVA/UVB light in the untreated areas of nine patients with CLE; no specific eruptions or any sun damage was observed in the sunscreen‐treated areas in any of the CLE patients, nor in the HCs. Histological analysis of skin biopsy specimens confirmed the clinical results. In conclusion, the use of a high‐protection, broad‐spectrum sunscreen can prevent UV‐induced damage in patients with CLE and HCs.     

Relevant new insights into the effects of photoprotection in cutaneous lupus erythematosus

Cutaneous lupus erythematosus (CLE) denotes a heterogeneous spectrum of autoimmune diseases that primarily affect the skin. Ultraviolet irradiation (UV) is one of the most important environmental factors that can trigger skin lesions in CLE or even induce systemic organ manifestation. It has been shown that broad‐spectrum sunscreen with high sun protection factors can effectively prevent UV‐induced skin lesions in patients with different subtypes of CLE. In a recent issue of Experimental Dermatology, Zahn and colleagues demonstrate that potent photoprotection blocks disease‐specific skin lesions in CLE patients by reducing lesional tissue damage and interferon‐driven inflammation.     

Type I interferon-associated skin recruitment of CXCR3+ lymphocytes in dermatomyositis

BACKGROUND: Dermatomyositis (DM) is an autoimmune disease of unknown origin affecting skin and muscles. Infiltrating autoreactive T lymphocytes are thought to play an important pathogenetic role, but it is unclear which mechanisms are involved in the recruitment of these cells. Recent studies provided evidence that a type I interferon (IFN)-driven immune response, including the recruitment of T cells via IP10/CXCR3 interactions, might be important for the generation of skin lesions of cutaneous lupus erythematosus (CLE), an autoimmune disease that shares some clinical and histopathological features with DM. We hypothesized that a similar mechanism might also be involved in the pathogenesis of DM skin lesions. METHODS: Skin biopsies of 23 donors (11 DM, 5 healthy controls, 7 CLE controls) were analysed by immunohistochemistry using monoclonal antibodies against CD3, CD4, CD8, CD20, CD68, CD123, the chemokine receptor CXCR3 and its ligand IP10/CXCL10, and the myxovirus-resistance protein A (MxA)-protein, which is a specific marker for type I IFNs. RESULTS: We detected strong expression of the MxA protein in all DM skin biopsies, indicating involvement of type I IFNs. Expression of MxA was closely associated with expression of the interferon-inducible protein IP10/CXCL10 and the recruitment of CXCR3+ lymphocytes. Plasmacytoid dendritic cells appear to be an important source of type I IFNs in DM. DISCUSSION: Our results support the hypothesis that lesional type I IFN signalling, induction of IP10 expression, and recruitment of potentially autoreactive T cells via IP10/CXCR3 interaction are involved in the pathogenesis of DM skin lesions.     

p53 labeling index in assessing the efficacy of a sunscreen in protection against UV‐induced damage

Background Sunscreen efficacy is currently evaluated by the estimation of the sun protection factor (SPF). Our objective was to determine the role of the p53 labeling index in assessing the effectiveness of a sunscreen in the prevention of UV‐induced DNA damage. Methods A broad‐spectrum sunscreen (SPF15) was applied to two of four test areas on the backs of 20 volunteers. Two test areas (with and without prior sunscreen application) were then irradiated with two minimal erythemal doses (MEDs) of solar‐simulated UV radiation (290–400 nm). At 24 h, suction blisters were raised from all four test areas using a vacuum technique, and immunohistochemical staining for p53 was performed. Results In normal epidermis, nonirradiated without sunscreen, p53 was almost undetectable [0.5% positive cells per field (PC/F)]. In UV‐exposed skin without sunscreen, p53 expression was 10.4% PC/F, whereas, in skin treated with sunscreen before UV irradiation, p53 expression was 0.3% PC/F. The mean positive labeling indices (×10³/µm) for UV‐exposed skin with and without sunscreen were 0.002 and 0.059, respectively (P < 0.001). Conclusions In vivo assessment of the p53 labeling index using the suction blister method can serve as a sensitive endpoint in the evaluation of the effectiveness of a sunscreen in the prevention of UV‐induced DNA damage.     

Apoptotic signal molecules in skin biopsies of cutaneous lupus erythematosus: analysis using tissue microarray

Cutaneous lupus erythematosus (CLE) is a heterogeneous autoimmune disease. Different pathogenetic mechanisms, including the accumulation of apoptotic keratinocytes in CLE, have been reported. Therefore, we investigated whether CLE and other inflammatory skin diseases differ with regard to the epidermal expression of molecules that are crucial for the initiation and regulation of apoptosis. In this study, 241 skin biopsies from patients with CLE, psoriasis (PSO), lichen planus (LP) and healthy controls (HCs) were analysed immunohistochemically using the tissue microarray (TMA) technique. The TUNEL assay and anti‐activated caspase‐3 antibodies revealed a significant increase of apoptotic keratinocytes in CLE lesions compared with HCs. Furthermore, we detected a significant increase in the epidermal expression of CD95 in CLE specimens compared with PSO, LP and HCs. These data suggest that the accumulation of apoptotic keratinocytes in CLE might be due to the increased epidermal expression of CD95, resulting in increased activity of the extrinsic apoptotic pathway in the disease.     

Expression of interleukin-17 is correlated with interferon-α expression in cutaneous lesions of lupus erythematosus

Background. Type I interferon (IFN) has been reported to have an important role in the development of cutaneous lupus erythematosus (CLE) and systemic lupus erythematosus (SLE). A new subset of CD4+ T cells, T helper (Th)17 cells, also plays a role in the development of autoimmunity. Aim. To investigate expression of interleukin (IL)‐17 and IFN‐α in different CLE subsets, and their associations with the pathogenesis of LE. Methods. Skin tissue samples from 33 cases, including chronic discoid LE (n = 24), acute (A)CLE (n = 4), subacute CLE (n = 1) and lupus panniculitis (n = 4) were collected for immunohistochemistry. Expression of IL‐6, IL‐17A, IFN‐α, IFN‐γ, myxovirus protein (Mx)A and transforming growth factor (TGF)‐β was assessed in these samples. Results. All LE specimens had staining for IL‐6 and TGF‐β in the infiltrated inflammatory cells. IL‐17A staining was seen in 84.8% of specimens, and IFN‐α or MxA was seen in 93.9%. TGF‐β expression in ACLE was significantly greater than that in both chronic cutaneous (CC)LE and in lupus panniculitis (P = 0.02 for both). Expression of IL‐17A was positively associated with expression of IFN‐α and MxA (Spearman’s ρ = 0.56 and 0.39, respectively). In addition, the Cutaneous Lupus Erythematosus Disease Area and Severity Index (CLASI) correlated positively with expression of IFN‐α and MxA (ρ = 0.40 for both), whereas there was no correlation with IL‐17A expression. Conclusions. Two major cytokines, IL‐17A and IFN‐α, may play roles in the pathogenesis of CLE. Their patterns of expression positively correlated with each other.     

Increased expression of guanylate binding protein-1 in lesional skin of patients with cutaneous lupus erythematosus

The large GTPase human guanylate binding protein-1 (GBP-1) is a key mediator of angiostatic effects of inflammation and is induced by interferon (IFN)-α and IFN-γ in endothelial cells (ECs). The aim of this study was to investigate whether GBP-1 is a marker of skin lesions in patients with cutaneous lupus erythematosus (CLE). Western blotting revealed that GBP-1 was in vitro induced by IFN-α and -γ in primary keratinocytes obtained from healthy controls. Moreover, we found that this protein was expressed by keratinocytes and ECs in primary and ultraviolet (UV)-induced skin lesions from patients with various subtypes of CLE, when compared to non-lesional skin. No GBP-1 expression was noted in skin biopsy specimens 24 or 72 h after UV irradiation prior to lesion formation in patients with CLE or in healthy control specimens with or without UV irradiation. Initial findings suggest that GBP-1 is not expressed in other skin diseases with different inflammatory aetiology, such as atopic dermatitis. We conclude that GBP-1 expression is closely associated with skin lesions in patients with CLE, suggesting a contribution of GBP-1 in the pathogenesis of this disease.     

Type 1 IFN-induced protein MxA and plasmacytoid dendritic cells in lesions of morphea

Morphea is an autoimmune sclerotic skin disease of unknown pathogenesis. As type 1 interferons (IFN) have been implicated in the pathogenesis of systemic sclerosis, we proposed that type 1 IFN promote localized inflammation and fibrosis in morphea. To investigate the expression of the type 1 IFN-inducible protein myxovirus A (MxA) and the presence of plasmacytoid dendritic cells (pDC) in lesions of morphea, lesional skin of 10 patients with morphea was examined by immunohistochemistry for the presence of the type 1 IFN-inducible protein, myxovirus A (MxA), and the pDC markers, CD123 and BDCA-2, and was compared with lesional skin of cutaneous lupus erythematosus, lichen planus and keloid. Lesional and non-lesional morphea skin was compared. MxA was expressed in the epidermis as well as the reticular dermis and subcutis in morphea. pDCs were abundant around vessels and between fibrous bundles. Non-lesional biopsies demonstrated little or no expression of MxA and pDC markers. Keloid showed minimal expression of MxA and pDC markers. We demonstrate the expression of type 1 IFN-related protein MxA and plasmacytoid DCs in lesional but not in non-lesional biopsies of morphea. These findings suggest a potential role for type 1 interferons in the pathogenesis of morphea.     

JAK inhibitor ruxolitinib inhibits the expression of cytokines characteristic of cutaneous lupus erythematosus

This study was stimulated by the clinical observation of a rapid response of a chilblain lupus patient to treatment with JAK1/2‐kinase inhibitor ruxolitinib. We investigated the in vivo expression of phospho‐JAK2 in CLE skin samples as well as the immunomodulatory in vitro effect of ruxolitinib in cultured immortalized keratinocytes and in a 3D human epidermis model (epiCS). Our results demonstrate that ruxolitinib significantly decreases the production of CLE‐typical cytokines (CXCL10, CXCL9, MxA) and might be a promising drug for future clinical studies in patients with CLE and related autoimmune skin diseases.     

Scarring skin lesions of discoid lupus erythematosus are characterized by high numbers of skin-homing cytotoxic lymphocytes associated with strong expression of the type I interferon-induced protein MxA

BACKGROUND: Infiltrating T lymphocytes are considered to play a major pathological role in skin lesions of cutaneous lupus erythematosus (CLE), a cutaneous autoimmune disease of unknown aetiology. Earlier histological studies revealed that the inflammatory infiltrate in CLE skin lesions is predominantly composed of T lymphocytes, with a slight predominance of CD4+ over CD8+ T cells, but failed to explain the development of scarring skin lesions, characteristic for chronic discoid lupus erythematosus (CDLE). Because recent investigations have highlighted the relevance of cytotoxic lymphocytes in autoimmune tissue destruction, we hypothesized that the scarring CDLE lesions might be caused by cytotoxic T lymphocytes. OBJECTIVES: To analyse skin biopsies of 15 patients with CLE [10 female, five male; localized CDLE (lCDLE), n = 5; disseminated CDLE (dCDLE), n = 5, subacute CLE (SCLE), n = 5] and five control biopsies taken from healthy controls and to characterize the inflammatory infiltrate. Methods We used immunohistochemistry, including staining for the cytotoxic molecule granzyme B, the skin-homing molecule cutaneous lymphocyte antigen (CLA) and the protein MxA, which is specifically induced by type I interferons (IFNs). RESULTS: We found a strong coexpression of granzyme B and CLA on lesional lymphocytes of patients with scarring lCDLE and dCDLE, which was significantly enhanced when compared with nonscarring SCLE and healthy controls. The increased expression of granzyme B was closely associated with the lesional expression of the type I IFN-induced protein MxA. CONCLUSIONS: Our results provide evidence that type I IFNs and potentially autoreactive cytotoxic lymphocytes targeting adnexal structures are highly associated with scarring lupus erythematosus lesions and might be responsible for their scarring character.     

Type I interferon-associated cytotoxic inflammation in lichen planus

INTRODUCTION: Lichen planus (LP) is an inflammatory autoimmune skin disease of unknown origin. Evidence has accumulated that autoreactive cytotoxic CD8(+) T lymphocytes cause destruction of keratinocytes. Recent studies suggested that type I interferons (IFNs) play a central role in cytotoxic skin inflammation by increasing the expression of IP10/CXCR10 and recruiting effector cells via CXCR3. Here, we investigated whether type I IFNs are also involved in the pathogenesis of LP. PATIENTS AND METHODS: Skin biopsies of altogether 17 donors (seven LP and 10 healthy controls) were analyzed by immunohistochemistry using monoclonal antibodies against CD3, CD4, CD8, CD20, CD68, CXCR3, granzyme B, IP10/CXCL10, CD123, and the MxA protein, which is specifically induced by type I IFNs. RESULTS: Our analysis revealed a significant expression of the MxA protein in all LP skin biopsies, indicating involvement of type I IFNs. Expression of MxA was closely associated with the recruitment of CXCR3(+) and granzyme B(+) lymphocytes, indicating a Th1-biased cytotoxic immune response. Strong expression of the CXCR3 ligand, the interferon-inducible protein IP10/CXCL10, links type I IFN expression and recruitment of CXCR3(+) lymphocytes. Plasmacytoid dendritic cells (pDCs) appear to be a major source of type I IFNs in LP. DISCUSSION: Our observations support the hypothesis that lesional type I IFNs produced by pDCs plays an important role in chronic cytotoxic inflammation of LP by recruiting cytotoxic effector lymphocytes via IP10/CXCR3 interactions.     

Update on the role of plasmacytoid dendritic cells in inflammatory/autoimmune skin diseases

Plasmacytoid dendritic cells (pDCs) represent a specialized dendritic cell population that exhibit plasma cell morphology, express CD4, CD123, blood‐derived dendritic cell antigen‐2 (BDCA‐2) and Toll‐like receptor (TLR)7 and TLR9 within endosomal compartments. When activated, pDCs are capable of producing large quantities of type I IFNs (mainly IFN‐α/β), which provide antiviral resistance and link the innate and adaptive immunity. While generally lacking from normal skin, pDCs infiltrate the skin and appear to be involved in the pathogenesis of several inflammatory, infectious (especially viral) and neoplastic entities. In recent years, pDC role in inflammatory/autoimmune skin conditions has been extensively studied. Unlike type I IFN‐mediated protective immunity that pDCs provide at the level of the skin by regulated sensing of microbial or self‐nucleic acids upon skin damage, excessive sensing may elicit IFN‐driven inflammatory/autoimmune diseases. In this review, focus will be on the role of pDCs in cutaneous inflammatory/autoimmune dermatoses.     

Protective effects of a topical antioxidant mixture containing vitamin C,ferulic acid,and phloretin against ultraviolet‐induced photodamage in human skin

Background Ultraviolet (UV) irradiation of the skin leads to acute inflammatory reactions, such as erythema, sunburn, and chronic reactions, including premature skin aging and skin cancer. Aim In this study, the effects of a topical antioxidant mixture consisting of vitamin C, ferulic acid, and phloretin on attenuating the harmful effects of UV irradiation on normal healthy volunteers were studied using biomarkers of skin damage. Subjects/methods Ten subjects (age, 18–60 years; Fitzpatrick skin types II and III) were randomized and treated with antioxidant product or vehicle control on the lower back for four consecutive days. On day 3, the minimal erythema dose (MED) was determined for each subject at a different site on the back. On day 4, the two test sites received solar‐simulated UV irradiation 1–5× MED at 1× MED intervals. On day 5, digital images were taken, and 4‐mm punch biopsies were collected from the two 5× MED test sites and a control site from each subject for morphology and immunohistochemical studies. Results UV irradiation significantly increased the erythema of human skin in a linear manner from 1× to 5× MED. As early as 24 h after exposure to 5× MEDs of UV irradiation, there were significant increases in sunburn cell formation, thymine dimer formation, matrix metalloproteinase‐9 expression, and p53 protein expression. All these changes were attenuated by the antioxidant composition. UV irradiation also suppressed the amount of CD1a‐expressing Langerhans cells, indicating immunosuppressive effects of a single 5× MED dose of UV irradiation. Pretreatment of skin with the antioxidant composition blocked this effect. Conclusion This study confirms the protective role of a unique mixture of antioxidants containing vitamin C, ferulic acid, and phloretin on human skin from the harmful effects of UV irradiation. Phloretin, in addition to being a potent antioxidant, may stabilize and increase the skin availability of topically applied vitamin C and ferulic acid. We propose that antioxidant mixture will complement and synergize with sunscreens in providing photoprotection for human skin.     

Synergistic effect of broad-spectrum sunscreens and antihistamines in the control of idiopathic solar urticaria

BACKGROUND: It can be difficult to provide patients with idiopathic solar urticaria adequate protection from sunlight. In a nonrandomized controlled trial, we used a standardized phototest procedure to determine the effects of using sunscreen and antihistamine to control idiopathic solar urticaria. OBSERVATIONS: Three patients with idiopathic solar urticaria underwent phototesting with UV-B and UV-A radiation. The minimal urticarial dose (MUD) was determined 15 minutes after irradiation. The patients were subsequently tested with 5 times the MUD, and the reaction was graded every minute for 15 minutes. The patients were then treated with a high-protection, broad-spectrum sunscreen and a nonsedative antihistamine alone and in combination and underwent similar phototesting. The use of sunscreen allowed the patients to tolerate much higher doses of UV radiation (32-38 times the MUD on untreated skin). Antihistamine use did not increase the patients' MUD but did suppress wheal formation and itch, and only immediate erythema sharply located in the irradiated areas occurred. The combination of sunscreen and antihistamine acted synergistically and increased the tolerance to UV radiation markedly (80-267 times the MUD on untreated skin). Conclusion High-protection, broad-spectrum sunscreens and antihistamines protect patients with solar urticaria in different ways and are highly effective when combined.     

Blue light irradiation suppresses dendritic cells activation in vitro

Blue light is a UV‐free irradiation suitable for treating chronic skin inflammation, for example, atopic dermatitis, psoriasis, and hand‐ and foot eczema. However, a better understanding of the mode of action is still missing. For this reason, we investigated whether dendritic cells (DC) are directly affected by blue light irradiation in vitro. Here, we report that irradiation neither induced apoptosis nor maturation of monocyte‐derived and myeloid DC. However, subsequent DC maturation upon LPS/IFNγ stimulation was impaired in a dose‐dependent manner as assessed by maturation markers and cytokine release. Moreover, the potential of this DC to induce cytokine secretion from allogeneic CD4 T cells was reduced. In conclusion, unlike UV irradiation, blue light irradiation at high and low doses only resulted in impaired DC maturation upon activation and a reduced subsequent stimulatory capacity in allogeneic MLRs with strongest effects at higher doses.     

Sun protection factor persistence during a day with physical activity and bathing

Background/purpose: The persistence of sunscreens during a day with physical activity and bathing is often debated. We wished to examine the durability of the protection achieved by one sunscreen application. Methods: Seven areas were marked on the back of 24 volunteers. One area was phototested to determine UV sensitivity. Six areas were treated with either an organic or an inorganic sunscreen (2 mg/cm²). The participants performed physical activities, were exposed to a hot environment and bathing during 8 h and were phototested with ultraviolet‐B (UVB) radiation 30 min, 4 and 8 h after sunscreen application. The minimal erythema dose (MED) was determined 24 h after irradiation. The sun protection factor (SPF) was calculated, as MED on protected skin/MED on unprotected skin. Results: The SPFs of the inorganic and organic sunscreen, respectively, were reduced by 38% and 41% after 4 h and by 55% and 58% after 8 h. Conclusion: One application of either an inorganic or an organic sunscreen reduced the erythema caused by UVB during a day with physical activity and bathing. After 8 h the sunscreens still provided approximately 43% of the initial protective effect. This might simulate what happens during a day at the beach.     

Sun exposure rapidly reduces plasmacytoid dendritic cells and inflammatory dermal dendritic cells in psoriatic skin

Background Interferon (IFN)‐α‐producing plasmacytoid dendritic cells (pDCs), inflammatory CD11c+CD1c? myeloid dendritic cells (mDCs) and macrophages have been found to contribute to the pathogenesis of psoriasis. Heliotherapy is a well‐established treatment modality of this disease, although the details of how the effects are mediated are unknown. Objectives To test the hypothesis that exposure to natural sun affects pathogenic DC subsets in lesional skin. Methods Skin biopsies were obtained from lesional and nonlesional skin in 10 patients with moderate to severe psoriasis subjected to controlled sun exposure on Gran Canaria. Biopsies were obtained at baseline, day 2 and day 16 and examined by immunohistochemistry. Results  Sixteen days of heliotherapy had excellent clinical effect on patients with psoriasis, with significant reductions in Psoriasis Area and Severity Index (PASI) scores. In lesional skin pDC numbers and expression of MxA, a surrogate marker for IFN‐α, were rapidly reduced. Inflammatory CD11c+CD1c? mDCs were significantly reduced whereas resident dermal CD11c+CD1c+ mDCs were unaffected. Expression levels of the maturation marker DC‐LAMP (CD208) on mDCs were significantly reduced after sun exposure, as were the numbers of lesional dermal macrophages. A decrease of dermal DC subsets and macrophages was already observed after 1 day of sun exposure. An additional finding was that DC‐SIGN (CD209) is primarily expressed on CD163+ macrophages and not DCs. Conclusions The clinical improvement in psoriasis following sun exposure is associated with rapid changes in dermal DC populations and macrophages in lesional skin, preceding the clinical effect. These findings support the concept that these DC subsets are involved in the pathogenesis of psoriasis and suggest that sun‐induced clinical benefit may partly be explained by its effect on dermal DCs.     

Spleen tyrosine kinase (SYK) is a potential target for the treatment of cutaneous lupus erythematosus patients

Spleen tyrosine kinase (SYK) is a protein kinase involved in cell proliferation and the regulation of inflammatory pathways. Due to the increasing evidence that kinase inhibitors have potential as specific anti‐inflammatory drugs, we have investigated the potential for SYK inhibition as a therapeutic target in autoimmune diseases, particularly cutaneous lupus erythematosus (CLE). Skin samples of patients with different CLE subtypes and appropriate controls were analysed for the expression of SYK and SYK‐associated pro‐inflammatory mediators via gene expression analysis and immunohistochemistry. The functional role of SYK in keratinocytes was investigated in vitro, using LE‐typical pro‐inflammatory stimuli and a selective inhibitor of SYK. SYK‐associated genes are strongly upregulated in CLE skin lesions. Importantly, phosphorylated SYK (pSYK) is strongly expressed by several immune cell types and also keratinocytes in CLE skin. In vitro, immunostimulatory nucleic acids are capable of inducing SYK phosphorylation in keratinocytes leading to the induction of pro‐inflammatory cytokines, while small‐molecule SYK inhibition decreases the expression of these proteins. The results demonstrate that pSYK is expressed by immune cells and keratinocytes in skin lesions of CLE patients. LE‐typical stimuli induce the expression of pSYK in vitro. Small‐molecule SYK inhibition leads to a reduction of pSYK expression and downregulation of pro‐inflammatory cytokines in keratinocytes. We therefore believe that pSYK provides a potential future drug target for the treatment of patients who suffer from CLE and related skin disorders. Specifically, our study reveals evidence supporting the use of topical SYK inhibitors in treating lupus.     

Evaluation of the capacity of sunscreens to photoprotect lupus erythematosus patients by employing the photoprovocation test

Although sunscreens are widely used to photoprotect patients with photosensitive lupus erythematosus (LE), standardized controlled studies that can prove their efficacy for this indication have been lacking. Therefore, in the present study, the capacity of three different, commercially available sunscreens to prevent the development of skin lesions that have been induced in LE patients under standardized, reproducible conditions by employing a provocative phototest was assessed. In a double blind, intraindividual comparative study, 11 patients with LE were photoprovoked according to a standard protocol. All patients developed LE-specific skin lesions upon photoprovocation with a combination of UVA plus UVB radiation. Each of the sunscreens tested prevented the development of skin lesions in this assay, but to various extents. Suncreen A (UVB: Octocrylene; UVA: Mexoryl SX, Mexoryl XL, Parsol 1789; TiO2) was by far the most effective by protecting in 11/11 patients. This protective capacity was corroborated by studies in which strong ICAM-1 mRNA expression was found in unprotected test areas, but not in sunscreen A pretreated sites. In contrast to sunscreen A, sunscreen B (UVB: Eusolex 6300, Parsol MCX, Uvinul T150, Neohelipan; UVA: Parsol 1789; TiO2) protected in 5 patients and sunscreen C (Eusolex 6300, Parsol MCX, Uvinul T150; UVA: Parsol 1789; TiO2) in 3 out of 11 patients. These studies indicate that the use of sunscreens is beneficial to LE patients because it can prevent the development of UV radiation-induced skin lesions. Effective protection, however, might vary considerably between different sunscreens.